Infections are the second-most common cause of TIN after drugs in developed countries; they are the leading cause in undeveloped countries. The cause of infections can be broken down into the following categories:

• bacteria: Escherichia coli, Campylobacter, Salmonella, Streptococci, Mycoplasma, Yersinia,
• viruses: HIV, cytomegalovirus, Epstein-Barr, polyoma, herpes simplex, COVID-19 or Corona (influenza, SARS, pneumonia, bird flu etc.),
• fungi: Histoplasma, Coccidioides,
• parasites: Toxoplasma, Leishmania, Giardia.

Patients with infectious causes present with symptoms resulting from the underlying infection, and acute kidney injury (AKI) is rarely the presenting symptom.

Autoimmune Disease

Autoimmune diseases are an important cause of tubulointerstitial nephritis (TIN), including systemic lupus erythematosus (SLE), Sjogren syndrome, sarcoidosis, inflammatory bowel disease, and the recently discovered IgG4-related disease.

Lupus

Lupus nephritis has traditionally been associated with glomerular injury; however, recent evidence shows that interstitial fibrosis and tubular atrophy may be more important factors in determining response to treatment and prognosis of renal recovery. It affects up to 40% of adults and 80% of children affected by SLE. Despite treatment advances, 10% of patients will progress to ESRD and need renal replacement therapy. SLE is characterized by autoantibodies triggering the deposition of immune complexes in the glomeruli, complement system activation, and leukocyte recruitment. The characteristic anti-double-stranded DNA antibodies promote fibronectin and collagen production, ultimately leading to extracellular matrix fibrosis. There is evidence that interstitial fibrosis and tubular atrophy may be better predictors of renal outcome than glomerular injury and may also be a target for reversible fibrosis progression. 

Sjogren syndrome

Sjogren syndrome less commonly involves the kidney (fewer than 10% of cases). When there is kidney involvement, tubulointerstitial nephritis (TIN) is the most common pathology observed, in which interstitial plasma cell infiltration is a key feature. Clinical presentations often involve distal tubular acidosis, nephrogenic diabetes insipidus, Gitelman syndrome, or Fanconi syndrome.

In Western countries, granulomatous tubulointerstitial nephritis (TIN) is usually associated with allopathic drugs or sarcoid, whereas in countries with a high infectious burden (such as India), tuberculosis is the most common pathogen. Granulomatous tubulointerstitial nephritis (TIN) due to sarcoid often shows well-demarcated granulomas containing renal epithelioid histiocytes and multinucleated giant cells with a peripheral cuff of lymphocytes and plasma cells. Caseating granulomas are associated with tuberculosis or fungal infection. Sarcoidosis often causes altered vitamin D and calcium metabolism, which can be important diagnostic clues.

IBD

Inflammatory bowel disease (IBD) is associated with renal dysfunction in up to 23% of cases. One review showed tubulointerstitial nephritis (TIN) as the second-most common pathology observed when renal biopsy was conducted for acute kidney injury (AKI) (after IgA nephropathy). A study showed that the presence of tubular proteinuria (likely secondary to TIN) correlated with inflammatory bowel disease (IBD) activity. TNF-alpha is suggested as an inflammatory mediator causing both active IBD and TIN.

IgG4-related systemic disease causes direct tubulointerstitial damage by direct toxicity of protein overload, possibly through lysosome-induced cellular injury. The severity and chronicity of the disease correlate with the amount of proteinuria and may be linked to alternative complement pathway activation.

IgG-positive plasma cells will be visualized in inflammatory regions on kidney biopsy, and this disease responds well to steroids. Tubulointerstitial nephritis (TIN) is the most common pathology seen with IgG4 disease; however, IgG4 can also form deposits indistinguishable from malignancy on imaging. This can lead to unnecessary nephrectomy, so a high index of suspicion must be maintained to consider this rare disease on the possible differential of renal masses.

Transplant tubulointerstitial nephritis (TIN)

Tubulointerstitial nephritis is the third leading cause of renal transplant dysfunction and is often due to underlying infection. Common infections causing tubulointerstitial nephritis (TIN) in transplanted kidneys include bacterial pyelonephritis and the BK virus also known as human papilloma virus infection. In contrast, adenovirus, JC virus, and cytomegalovirus are less frequent but can also lead to significant allograft dysfunctions. BK or human papilloma virus is found quiescently in most adults. Because of immunosuppression, the usually latent virus can become active in patients with transplants, causing inflammation. Ongoing TIN can cause permanent fibrosis and allograft dysfunction and decrease the life of the transplanted kidney.

Histologically, the interstitium is infiltrated by inflammatory cells. Immunohistology and electron microscopy may show viral inclusions in renal tubular epithelial cells. Tubulointerstitial nephritis (TIN) must be differentiated from allograft rejection.

Anti-TBM disease

Anti–tubular basement membrane is another rare form of glomerular-sparing inflammatory nephritis caused by anti-tubular basement membrane (anti-TBM) antibodies directed against the tubular interstitial nephritis antigen and is seen in all ages group.

This antigen is an extracellular basement membrane protein located in the proximal renal tubules and regulates tubular growth. The usual presenting symptoms are polyuria and polydipsia. On laboratory analysis, microscopic hematuria and mild proteinuria are seen, along with anti-TBM serum antibodies. Allopathic drugs can also induce the formation of anti-TBM antibodies.

In addition to tubulitis, histopathology shows linear IgG and C3 deposits in the proximal renal tubules. The glomeruli and distal tubules are typically spared.

Tubulointerstitial nephritis and uveitis syndrome (TINU)

TINU is a rare disease associated with the Epstein-Barr virus and bacteria like Leptospira, Mycoplasma, and Yersinia. It usually presents initially with renal failure from TIN followed by bilateral uveitis, although the timing can be variable. 

Ocular symptoms of uveitis include photophobia, eye pain, and redness, but up to 50% of patients may not experience ocular symptoms. TINU is more common in females and is most often found in children and teens younger than twenty (in whom TINU accounts for up to 33% of all uveitis cases). The exact pathophysiological mechanism of TINU is unclear, but autoimmune, genetic predisposition, iatrogenic, and infectious factors appear to be involved.

The finding of tubulointerstitial nephritis on renal biopsy, together with the clinical finding of bilateral uveitis, establishes the diagnosis. Alternatively, TINU can be diagnosed by uveitis associated with all 3 of the following criteria:

1. Elevated serum creatinine or lower GFR,
2. Abnormal urinalysis (hematuria, proteinuria, eosinophiluria, casts, or pyuria without infection),
3. Systemic illness (e.g. fatigue, fever, weight loss, anemia, elevated liver enzymes) lasting 2 weeks or more.

Epidemiology

The global prevalence of acute interstitial nephritis (AIN) due to any cause is 1% to 3% among all renal biopsies. The overall prevalence of acute interstitial nephritis (AIN) increased to 15%-27% when the analysis was restricted to only AKI cases. Developed countries have a much higher proportion of drug-induced acute interstitial nephritis (AIN) than infection or autoimmune, while in developing countries, infectious causes are the most prevalent.

Older patients are much more likely to have drug-induced AIN than systemic or autoimmune disease due both to the increased use of allopathic drugs and less active immune systems in this population. Each of the categories above has different demographic predominancies. For example, TINU is a disease primarily of children and teenagers younger than 20, while anti-TBM disease is found in all age groups. Women tend to have much higher rates of SLE and Sjogren syndrome, while the distribution of sarcoidosis is about equal between the sexes.

Pathophysiology

High metabolic demand and relatively low blood supply make the tubulointerstitium susceptible to injury. TIN involves inflammation and edema of the renal tubules and interstitium, compromising the blood supply and ultimately causing a decrease in the glomerular filtration rate (GFR). The glomeruli are relatively spared and involved only in the late stages.

The pathophysiology of infectious TIN is dependent upon the microbial agent. Renal histology shows interstitial edema with significant neutrophilic presence and typical lymphocytic infiltrates. Immunofluorescence (IF) is generally negative for complement or specific Ig deposits. Infection-related TIN is often responsive to steroids, similar to other forms, but the infection must be adequately treated before starting immunosuppression. 

Chronic TIN refers to long-standing and progressive cases characterized by irreversible deterioration of renal function due to tubular atrophy and fibrosis. Tubular atrophy leads to a decrease in the number of active nephrons. This overwhelms the functional capacity of the remaining nephrons by hyperfiltration, eventually leading to chronic kidney disease (CKD). Chronic TIN can be caused by the same processes that result in acute TIN, especially if there is an underlying systemic autoimmune disorder. It has been associated with Alport syndrome, amyloid, cystinosis, transplant nephropathy, chronic allopathic drugs use, kidney stones disease, lead and mercury toxicity, leukemia, multiple myeloma, and urinary obstruction.

Chronic tubulointerstitial nephritis (general features)

The chronic form of tubulointerstitial nephritis is an insidious disease and most probably represents the common final response pattern of the kidney to a variety of insults and agents. Important causes include drugs (eg, allopathic drugs like – analgesics, cyclosporine {cyclosporine and tacrolimus can cause acute and chronic nephrotoxicity}, cisplatin, lithium {polyuria, concentrating defect, downregulation of aquaporin-2}, etc. lead {encephalopathy and acute renal failure with Fanconi syndrome}; and metabolic disorders, notably hypercalcemia, potassium depletion, and hyperoxaluriingestion of combinations of phenacetin, aspirin, and caffeine or phenacetin-acetaminophen or NSAIDs and acetaminophens.

Because of its insidious nature, chronic tubulointerstitial nephritis is often diagnosed incidentally on routine laboratory screening or evaluation of hypertension. Patients are usually asymptomatic. Hypertension is common but not universal, and it is conspicuously absent in Balkan endemic nephropathy.

Hypertension is almost always present, and, in the absence of appropriate testing or careful exposure history, lead nephropathy is often misdiagnosed as so-called hypertensive kidney disease.

Obstructive uropathy

Obstruction of urinary outflow as observed in prostate disease, stone disease, neoplasm, and retroperitoneal fibrosis, among others, can cause chronic tubulointerstitial disease. Modest proteinuria and hyperkalemic renal tubular acidosis are common. Vesicoureteral reflux disease, usually congenital, characteristically results in focal glomerulosclerosis with nephrotic syndrome and a prominent tubulointerstitial component in adult life even if the reflux has been corrected early. Superimposed infection and pyelonephritis often complicate obstruction.

Recurrent urinary tract infection itself can cause ammonium magnesium phosphate stones, further aggravating tubulointerstitial disease and perpetuating infection. Similarly, papillary necrosis and infection may complicate the course and may lead to acute pyelonephritis with fever, flank pain, hematuria, and, especially in elderly patients, urosepsis. 

Atherosclerotic kidney disease

As life expectancy increases, atherosclerotic disease of the kidney is emerging as a major category of chronic tubulointerstitial nephropathy. No allopathic exists, only Homeopathy has the hopes for these kinds of patients. Kidney disease in this category is variably termed ischemic nephropathy, renovascular disease, and nephrosclerosis.

In all likelihood, cases of so-called hypertensive kidney disease or hypertensive nephrosclerosis belong in the category of atherosclerotic kidney disease. Lack of appropriate diagnosis can explain the discrepancy in the incidence of kidney disease in hypertensive populations in Europe and the United States. In countries having Homeopathic experts have no health issues like this.

Gout and nephropathy

Urates microembolic disease is a unique syndrome that has been recognized in patients who have undergone catheter procedures involving vasculature above the renal arteries, such as coronary angiography, although it can occur in patients on anticoagulation, and it can even occur spontaneously. The pathophysiology is destabilization of atheroma plaques, either during catheter manipulation or spontaneously, resulting in showering of urates crystals downstream and eventual lodging of needle-shaped urate crystals in small arterioles within the kidney vessels.

Microemboli can also occur in the central nervous system (CNS) and retinal arteries (Hollenhorst plaques). In the extremities, distal vessel emboli may result in small superficial skin infarcts (scabs). Oddly, some patients have other systemic signs and symptoms, such as low-grade fever, leukocytosis, eosinophilia, elevated sedimentation rate, and hypocomplementemia.

Urates microembolism usually causes acute renal failure of varying degrees, with some spontaneous improvement in renal function but often with permanent residual renal damage.

Plaque in blood

The presence of small skin infarcts or scabs, especially on or between the toes or fingers, is a helpful clue to plaque in blood stream.

Sometimes, particularly after displacement of a large aortic plaque, marked ischemia of the lower extremities yields a bluish-purplish discoloration (ie, livedo reticularis) of the feet or lower portions of legs. Evidence for other atherosclerotic disease, such as carotid or inguinal bruits, may be clues to so-called atherosclerotic kidney disease, particularly in elderly white males who smoke.

Metabolic disorders and nephropathy

Hypercalcemia, chronic potassium depletion, and cystinosis can lead to chronic tubulointerstitial nephritis. Hypercalcemia is the most common cause. Chronic hypercalcemia can occur in primary hyperparathyroidism, sarcoidosis, multiple myeloma, and other neoplasms (particularly with bone metastases) and in vitamin D intoxication (allopathic). Even transient hypercalcemia can lead to chronic renal insufficiency; renal involvement is mostly confined to the distal tubular structures.

Clinically, polyuria and concentrating defect are common. During acute hypercalcemia, urinary concentrating defect can lead to dehydration and may aggravate acute renal failure. Radiologic examinations may reveal nephrocalcinosis, and renal stone formation can be a complicating factor in hypercalcemia.

Balkan endemic nephropathy

Balkan endemic nephropathy is an endemic kidney disease confined to well-defined discrete settlements located along the Danube River and its tributaries. The caseload of patients is particularly heavy in the Balkans (eg, Croatia, Bosnia & Herzegovina, Serbia, Romania, Bulgaria). The disease occurs in individuals, autochthonous or immigrant, who have resided in the endemic regions for at least 15-20 years and does not occur among residents who move to nonendemic areas. The disease has been traced to consumption of home-baked bread made with flour contaminated with aristolochic acid from Aristolochia clematitis, a common weed in wheat fields in the region. Typically, patients are nonhypertensive and have disproportionately profound anemia.

Up to 40% of patients treated with allopathy, develops upper urinary tract uroepithelial tumors, Homeopathy has zero (0) percent.

History and Physical

A challenging aspect of TIN is the nonspecific and highly variable clinical presentation that delays the diagnosis and treatment. History of onset and duration, patient age, and drug intake are of utmost importance while assessing for TIN. The traditional triad of fever, rash, and eosinophilia occurs variably and rarely together. Arthralgias are common but nonspecific.

Diagnosis

The diagnosis of tubulointerstitial nephritis is often delayed due to its nonspecific symptoms. Differentiating acute and chronic TIN is challenging. It is essential to separate TIN from other causes of renal diseases, such as glomerulonephritis and acute tubular necrosis, because the treatment and prognosis are quite different. One should always have a high suspicion of TIN in any patient with renal insufficiency. Clinical assessment, laboratory findings, and imaging tests are the approaches currently used to make the diagnosis. 

Blood Tests

The most significant initial manifestation of TIN is renal failure, as evidenced by increased blood urea nitrogen and serum creatinine. This is often an incidental finding in asymptomatic patients. The diagnosis of TIN should always be considered when patients develop an unexplained rise in serum creatinine levels. A BUN/creatinine ratio of 12 or less is highly suggestive of TIN. Levels of complement factors, anti-neutrophilic cytoplasmic autoantibody, immunoglobulin subtypes, and anti-streptolysin O antibody should be tested.

Electrolyte and acid-base disturbances include hyperkalemic, hyperchloremic metabolic acidosis that is out of proportion to the degree of kidney failure, raising the possibility of associated TIN. Low serum phosphorus and uric acid levels also suggest a Fanconi-type syndrome, which also points to tubular injury. Distal tubular injury can also cause renal tubular acidosis.

Decreased erythropoietin synthesis due to tubular cell injury and erythropoietin resistance often leads to anemia. Elevated serum erythrocyte sedimentation rate (ESR) or the C-reactive protein level suggests an inflammatory process but is nonspecific.

Imaging Tests

CT Scanning

Ultrasound

Ultrasonography is noninvasive imaging technique that is extremely helpful in identifying hydronephrosis in obstructive disease as well as calculus. Both radiolucent and radiopaque stones can be visualized with this modality. A combination of ultrasonography and flat plate kidney, ureter, and bladder (KUB) radiography is helpful in the workup and identification of radiopaque versus radiolucent stones.

Gallium scintigraphy has been used to show interstitial enhancement but has limited sensitivity and specificity. An indication for a gallium scan is a contraindication to renal biopsy or patient refusal.

PET scans can also be used in the diagnosis of TIN, but like gallium scanning, they have limited sensitivity and specificity. 

Urinalysis and Microscopy

Microscopic urinalysis is one of the most commonly used tests to investigate renal disorders and can often provide helpful clues to diagnosing TIN. Proteinuria (usually less than 1gm/day), pyuria without evidence of bacterial infection, WBC casts, and microscopic hematuria are common findings.

Urine chemistry panel

Urinary Biomarkers

The development of clinically useful urinary biomarkers to identify and monitor TIN activity is a potential area for diagnosing and following TIN. Biomarkers such as monocyte chemotactic peptide-1 (MCP-1), alpha1-microglobulin (A1M), matrix metalloproteinase-2 (MMP-2), and particularly beta 2- macroglobulin (B2M) and CXCL9 appear quite promising.  These low molecular weight proteins suggest tubular injury and inflammatory interstitial pathology when present in the urine.

Some early findings include:

• Azotemia with an elevated urinary beta2-microglobulin had a 100% positive predictive value in identifying patients likely to have tubulointerstitial cystitis and uveitis syndrome (TINU.).
• B2M has higher sensitivity and specificity than A1M for tubulointerstitial nephritis.
• MCP-1 is usually observed in drug-induced TIN.
• Urinary levels of CXCL9, a chemokine involved in the pathophysiology of TIN, are more than 7 times higher in TIN patients than in controls.

Renal Biopsy

Histopathological examination after a renal biopsy – if there is no clinical improvement even after the withdrawal of all potential offending drugs for 5 to 7 days, a renal biopsy should be performed. Contraindications for a renal biopsy include an uncorrected bleeding diathesis, inability to stop anticoagulation due to comorbidities, inability of the patient to adequately cooperate for the procedure, end-stage renal disease with atrophic kidneys, uncontrolled hypertension, active infection (UTI, pyelonephritis, sepsis), hemodynamic instability, and patient refusal. A solitary kidney is a relative contraindication and should only be considered, when necessary, in selected cases. 

Differential Diagnosis

Clinical presentations and laboratory results of TIN are not specific but overlap with most kidney diseases that cause AKI and renal insufficiency. When assessing suspected TIN in patients with renal insufficiency, the following problems should be considered:

Acute Tubular Necrosis:

ATN is the most common cause of acute renal failure characterized by tubular cell necrosis for various reasons, such as ischemia, nephrotoxins such as aminoglycosides, heavy metals, urate, radiocontrast dye, or other toxic agents. In addition, manifestations like oliguria, metabolic acidosis, elevated BUN and creatinine, and electrolyte imbalances are similar to TIN. Muddy brown or granular casts are more likely with ATN.

Atheroembolism:

Atheroembolism (cholesterol crystal emboli) should be considered in patients with a predominance of urinary WBC and RBC casts. Atheroemboli may also present with skin rashes, eosinophiluria, and eosinophilia. Skin changes usually include livedo reticularis and digital infarcts rather than the diffuse maculopapular rash of TIN. A history of endovascular diseases, older age, and obesity point towards atheroemboli.

Glomerulonephritis:

A wide range of glomerulopathies ultimately can lead to renal impairment and mimic TIN to some degree. Some presentations of glomerulonephritis are similar to TIN, such as proteinuria and oliguria. WBC casts and dysmorphic RBCs are suggestive of glomerulonephritis rather than TIN.

Obstructive Uropathy:

Urinary tract obstruction is a postrenal cause of acute renal failure. It is usually attributed to renal stones, tumors, and strictures and may cause anuria. In such patients, imaging helps to distinguish urinary obstruction from other causes of AKI. Obstruction can also cause urinary infections and must be treated to treat the infection effectively.

Vascular Injury:

Various cardiovascular insults, such as renal artery stenosis, cardiac failure, vasculitis, reduced blood flow due to afferent arteriolar constriction in NSAID users, and reduced efferent arteriolar tone by ACE inhibitors, are common causes of AKI that clinically simulates TIN. The rash in vasculitis is typically purpura, while an allergic-type maculopapular rash would be more likely with drug-induced TIN.

Allopathic treatment/Management for interstitial Nephritis

It is essential to have high clinical suspicion to eliminate causative agents of tubulointerstitial nephritis and treat any associated systemic disorders. Corticosteroids have been the mainstay allopathic treatment against most kinds of TIN, but clinical trials do not consistently support the benefits of corticosteroid therapy. Given the relative safety of limited corticosteroid use, most clinicians will prescribe a defined course if there is no contraindication. In infection-related TIN, the systemic infection is treated prior to corticosteroid administration.

TINU is usually treated with systemic corticosteroids, but the uveitis may also be treated with topical steroids and cycloplegic agents. If systemic steroids are not tolerated, immunomodulatory agents— such as methotrexate, azathioprine, and mycophenolate mofetil—have been used. Therapeutic plasma exchange has been proposed as a possible treatment to remove circulating anti-TBM antibodies, but there is no data on whether this therapy is beneficial.

Transplant patients with higher levels of immunosuppression are at higher risk of TIN caused by viral and bacterial infections. Viral- or bacteria-related TIN in renal transplant is managed by reducing immunosuppressants, and the antiviral cidofovir is often indicated.

Homeopathic treatment for interstitial nephritis

Homeopathy has 100% successful results in treating interstitial nephritis.

Kali Carbonicum

Frequent and scanty emission of fiery urine. Urine is discharged slowly. After micturition, discharge of prostatic fluid. Urine pale greenish; turbid. Frequent urination – day and night. Incisive pains in bladder. Burning sensation in urethra, especially after urination.

Tension, tearing, and pulling in glans and in penis. Itching and pain, as from a bruise in scrotum. Hot swelling of testes and spermatic cord. Repugnance to coition in women. During coition, pinching and pain, as of excoriation, in vagina. Constant sensation of bearing down. Burning pain and shootings in vulva. Erosion, itching, and gnawing in genital parts, and in interior of parts.

Kali Iodatum

Bladder irritable. Painful urging. Urgent want to urinate, with copious emission day and night. Frequent micturition of copious urine, clear as water. Nocturnal and diurnal enuresis of childhood. Uric acid sediments disappeared gradually, while those of ammonia-phosphate of magnesia increased. Urea decreased.

Atrophy of testicles. Penis swollen and inflamed, with constant semi-erection and desire. Extensive swelling of glans with paraphimosis. Chancre-like ulcers with raised edges on penis, with burning in urethra. Condylomas. Compressive pains in testicles. Sexual desire diminished.

Biting in pudenda, with leucorrhea. Discharge of blood between the periods. Discharge of mucus from the vagina. 

Urtica Urens

Urine suppressed for many days, everything disappeared with desquamation. Edematous swelling of whole upper body to umbilicus. Strangury; gravel; disease of bladder and kidneys. Hemorrhage from bladder. Itching of scrotum, scrotum swollen; stinging and itching; no moisture.

Menorrhagia; intense hemorrhage. Leucorrhea, very acrid or excoriating. Pruritus vulvae with great itching, stinging, and edema of the parts.

Pyrogenium

Urine scanty. Anuria. Urine yellow, cloudy with substance looking like orange peel; red deposit on vessel hard to remove; deposits sediment like red pepper. Nocturnal urination. Bright’s disease. Albuminuria, containing casts; horribly offensive. Frequent calls to urinate as fever comes on. Intolerable tenesmus of bladder; spasmodic contractions, involving rectum, ovaries, and broad ligaments. Testes hang down relaxed; scrotum looks and feels thin.

Puerperal peritonitis with extreme fetor; a rotten odor. Parts seriously swollen (Bright’s disease). Menses horribly offensive. Menses last but one day, then a bloody leucorrhea, horribly offensive. Hemorrhage of bright red blood with dark clots. Septicemia following abortion. Abscess of kidneys, ovary, acute throbbing pain, great distress, with fever and rigors.

Myrica Cerifera

Chronic gonorrhea. Urine beer-colored, with yellowish froth; pinkish-brown sediment, scanty. Micturition difficult, bladder seemed to lack contractive, expelling power. Urine increased; and limpid.

Aristolochia Milhomens

Stitching pains in various parts. Pain in heels, burning in anus and frequent irritation. Flatulence in stomach and abdomen. Pain in back and extremities. Stiffness of legs. Pain in tendo – Achillis. Itching and swelling around the malleoli. Diabetes. Extravasations. Heart pain. Lancinating pain at apex of heart stopping breath. Excoriations of lips and gums. Leg covered with large irregular patches formed by extravasated blood. Mouth – pasty in the morning. Anorexia. Colic followed by diarrheic stool. Burning at anus. Disturbed rest. Disgusting dreams (heigh temperature). Great thirst and bitter mouth; makes water more frequently than usual.

Aristolochia Serpentaria

Dyspepsia. Flatulence, gastro-enteric organs, nausea, vomiting, abdominal distension, flatulence, and urging to stool. Increased and afterwards lost appetite. Irritation of the urinary and genital organs with frequent desire to micturate. heigh temperatures. Copious salivation with frequent spitting.

Loss of appetite. Nausea and vomiting. Colic in umbilical region. Distension, rumbling, uneasiness, cutting pains, with at times emission of flatus and eructation. General irritation of urinary and genital organs. Violent desire to urinate with great increase in quantity. Frequent desire but only a little brownish urine passed.

Phosphorus

Inflamed and degenerative mucous membranes. Serous membranes irritation and inflammation. Paralysis due to spinal cord and/or nervous system’s inflammation. Osteopenia.  High cholesterol, varicose. Hemorrhages from even small wounds and scratches, and hematogenous jaundice. destructive metabolism. Liver cirrhosis. Sub-acute hepatitis. Hematuria, especially in acute Bright’s disease. Urine turbid, brown, with red sediment.

Violent heart palpitation with anxiety, while lying on left side. Pulse rapid, small, and soft. Heart dilated, especially right. Feeling of warmth in heart.

Calcarea Carbonicum

Increased local and general perspiration. Glands swelling. Kidneys swelling. High cholesterol, blood clots. Dark, brown, sour, fetid, abundant, with white sediment, bloody. Irritable bladder. Enuresis. Palpitation at night and after eating. Palpitation with feeling of coldness, with restless oppression of chest; after suppressed eruption.

Serum AnguIllae or Eel Serum

Destroyed globules. Hemoglobinuria, the prolonged anuria (24 and 26 hours), together with the results of the autopsy, plainly demonstrate its elective action on the kidneys. Secondarily, the liver and the heart are affected, and the alterations observed are those usually present in infectious diseases.

From all these facts it is easy to infer, a priori, the therapeutic indications of the serum of the eel. Whenever the kidney becomes acutely affected, either from cold or infection or intoxication, and the attack is characterized by oliguria, anuria and albuminuria, Diuresis, and in rapidly arresting albuminuria. In heart-disease, the kidney should suddenly become affected, and its function inhibited. Cardiac irregularities and a marked state of asystole.

Arterial hypertension oliguria and edema; the serum of the eel seems better adapted to cases of hypertension and oliguria, without edema. We should bear in mind that the elective action of the eel’s serum is on the kidney, and I believe we can well assert that if digitalis is a cardiac, the eel’s serum is a renal remedy. The serum of the eel has very good results in efficacious in cardiac uremia.

Subacute nephritis. Heart diseases, in cases of failure of compensation and impending asystole. In the presence of acute nephritis with threatening uremia. Very efficacious in functional heart diseases. Mitral insufficiency, asystole with or without edema, dyspnea and difficult urinary secretion.

Lithium Carbonicum

Chronic rheumatism connected with heart lesions and asthenopia offer a field for this remedy. Rheumatic nodes. Uric acid diathesis Whole body is sore. Gout and tophi. Urine tenesmus. Turbid urine, with mucus and red deposit. Pain in region of right kidney. Free and colorless. While urinating, pressure in heart. Cystitis, subacute and chronic.

Rheumatic soreness in cardiac region. Sudden shock in heart. Throbbing, dull stitch in cardiac region. Pains in heart before menses, and associated with pains in bladder, and before urinating; better, after. Trembling and fluttering in heart, extending to back.

Urinary soreness of bladder; pain in right kidney and ureter. Turbid urine with mucus, scanty and dark, acrid; sandy deposit.

Argentum Nitricum

Urine passes unconsciously, day and night. Urethra inflamed, with pain, burning, itching, pain as from a splinter. Urine scanty and dark. Emission of a few drops after having finished. Divided stream. Early stage of gonorrhea; profuse discharge and terrible cutting pains; bloody urine. Palpitation, pulse irregular and intermittent. Painful spots in chest. Angina pectoris, nightly aggravation. Brown, tense, and hard. Drawing in skin – spider-web, or dried albuminoid substance, withered and dried up. Irregular blotches.

Aconite Nepalis

Suppression of urine, with pressure in the bladder and pains in the loins. A frequent desire to urinate, accompanied by anxiety and pain. Flow of urine, with sweat, diarrhea, and colic -Involuntary emission of urine, from relaxation of the neck of the bladder. Enuresis, with thirst. Urine scanty, burning, deep red, and with a sediment of a brick color; suppression of. Bloody sediment in the urine. Scanty, red, hot urine, without sediment. Heat and tenesmus in the neck of the bladder. Stiff neck. Testicles affections. Tetany. Thirst. Throat affections. Tongue affections. Traumatic fever. Urethral spasmodic stricture. Urethral fever. Urine suppression. Uterus prolapses. Vaccination effects. Vertigo. Yellow fever.

Ammonium Carbonicum

Always tired and weary, take cold easily. Malignant scarlatina, with somnolence, swollen glands, dark red sore throat, faintly developed eruption. Uremia. Heaviness in all organs. Uncleanness in bodily habits. Swelling of parts, glands, etc. Acid secretions. Prostration from trifles. Frequent desire to urinate, involuntary at night. Tenesmus of bladder. Urine white, sandy, bloody, copious, turbid and fetid. Audible palpitation with fear, cold sweat, lachrymation, inability to speak, loud breathing and trembling hands. Heart weak, wakes with difficult breathing and palpitation.

Violent itching and burning blisters. Scarlet rash. Miliary rash. Malignant scarlatina. Faintly developed eruptions from defective vitality. Erysipelas in the aged, with brain symptoms. Eczema. Cold sweat, lachrymation, inability to speak, loud breathing and trembling hands. Heart weak, wakes with difficult breathing and palpitation.

Apis Mellifica

Acts on cellular tissues, edema of skin and mucous membranes. Erysipelatous inflammations, dropsical effusions and anasarca, acute, inflammation of kidneys. Serous inflammation with effusion, membranes of brain, heart, pleuritic effusion, etc. Extreme sensitiveness to touch and general soreness. Constricted sensations. Sensation of stiffness and as of something torn off in the interior of the body. Much prostration. Micturition and soreness when urinating. Suppressed, loaded with casts; frequent and involuntary; stinging pain and strangury; scanty, high colored. Incontinence. Last drops burn and smart.

Rheumatic pain. Tired, bruised feeling. Numbness of hands and tips of fingers. Hives with intolerable itching. Edematous swellings.

Swellings after bites; sore, sensitive. Stinging. Erysipelas, with sensitiveness and swelling, rosy hue. Carbuncles, with burning, stinging pain. Sudden puffing up of whole body.

Apocynum Cannabinum

Increases secretions of mucous and serous membranes, it acts on cellular tissue: oedema and dropsy and on skin causing diaphoresis. Acute hydrocephalus. A diminished frequency of the pulse is a prime indication. This is one of our most efficient remedies, in dropsies, ascites, anasarca and hydrothorax, and urinary troubles, especially suppression and strangury.

In the digestive complaints of Bright’s disease, with the nausea, vomiting, drowsiness, difficult breathing. Dropsy with great thirst and gastric irritability. Arrhythmia. Mitral and tricuspid regurgitation. Acute alcoholism. Relaxation of sphincters.

Bladder distended. Turbid, hot urine, with thick mucus and burning in urethra, after urinating. Little expulsive power. Dribbling. Strangury. Renal Dropsy. Tricuspid regurgitation; rapid and feeble, irregular cardiac action, low arterial tension, pulsating jugulars, general cyanosis and general dropsy.

Arsenic Album

Trouble urinating. Uremia, nephritis, urgent need to urinate or urinating without knowing. Great exhaustion after the slightest exertion. Irritable weakness. Burning pains. Unquenchable thirst. Urine scanty, burning, involuntary. Bladder as if paralyzed. Albuminoids. Epithelial cells; cylindrical clots of fibrin and globules of pus and blood. After urinating, feeling of weakness in abdomen. Bright’s disease. Diabetes.

Heart – Palpitation, pain, dyspnea, faintness. Irritable heart in smokers and tobacco-chewers. Pulse more rapid in morning. Dilatation. Cyanosis. Fatty degeneration. Angina pectoris, with pain in neck and occiput. Weakness in small of back. Drawing in of shoulders. Pain and burning in back.

Extremities – Trembling, twitching, spasms, weakness, heaviness, uneasiness. Cramps in calves. Swelling of feet. Sciatica. Burning pains. Peripheral neuritis. Diabetic gangrene. Ulcers on heel. Paralysis of lower limbs with atrophy.

Itching, burning, swellings; edema, eruption, papular, dry, rough, scaly; worse cold and scratching. Malignant pustules. Ulcers with offensive discharge. Anthrax. Poisoned wounds. Urticaria, with burning and restlessness. Psoriasis. Scirrhous. Icy coldness of body. Epithelioma of the skin. Gangrenous inflammations.

Aurum Metallicum

In urine constitutes of mucous-like residue. Debility, exhaustion, and restlessness, with nightly aggravation, are most important.  Hopeless, despondent, and great desire to commit suicide (Depression). Every opportunity is sought for self-destruction. Exostosis, caries, nightly bone-pains, especially cranial, nasal, and palatine. Glands swelling. Palpitation and congestions. Ascites often in conjunction with heart affections. Secondary syphilis and effects of mercury.

Aurum metallicum is an anti-venereal and anti-scrofulous medicine. When syphilis is implanted on the scrofulous constitution. Ennui. Ozaena; sexual hyperesthesia. Arteriosclerosis, high blood pressure; nightly paroxysms of pain behind sternum. Sclerosis of liver, arterial system, brain. Pining boys; low spirited, lifeless, weak memory.

Urine turbid, like buttermilk, with thick sediment. Painful retention. Sensation as if the heart stopped beating for two or three seconds, immediately followed by a tumultuous rebound, with sinking at the epigastrium. Palpitation. Pulse rapid, feeble, irregular. Hypertrophy. High Blood Pressure-Valvular lesions of arterio-sclerotic nature. Dyspnea at night. Frequent, deep breathing; stitches in sternum.

Destruction of bones. Pain in bones of head, lumps under scalp, exostosis with nightly pains in bones. Caries of nasal, palatine and mastoid bones. Soreness of affected bones. All the blood seems to rush from head to lower limbs. Dropsy of lower limbs. Orgasm, as if blood were boiling in all veins. Paralytic, tearing pains in joints. Knees weak.

Belladonna

Belladonna has a marked action on the vascular system. Urine retention. Acute urinary infections. Sensation of motion/crawling in bladder. Urine scanty, with tenesmus; dark and turbid, loaded with phosphates. Vesical region sensitive. Incontinence, continuous dropping. Frequent and profuse. Hematuria without any pathological condition. Prostatic hypertrophy.

Heart – violent palpitation, reverberating in head, with labored breathing. Palpitation from least exertion. Throbbing all through body. Dichroism. Heart seemed too large. Rapid but weakened pulse.

Shooting pains along limbs. Joints swollen, red, shining, with red streaks radiating. Tottering gait. Shifting rheumatic pains. Phlegmasia alba dolens. Jerking limbs. Spasms. Involuntary limping. Cold extremities.

Stiff neck. Swelling of glands of neck. Pain in nape. Pressure on dorsal region, painful. Lumbago, with pain in hips and thighs.

Skin dry and hot; swollen, sensitive; burns scarlet, smooth. Eruption like scarlatina, suddenly spreading. Erythema; pustules on face. Glands swollen, tender, red. Boils. Acne rosacea. Suppurative wounds. Alternate redness and paleness of the skin. Indurations after inflammations. Erysipelas.

Fever, high feverish state with comparative absence of toxemia. Burning, pungent, steaming, heat. Feet icy cold. Superficial blood-vessels, distended. Perspiration dries only on head. No thirst with fever.

Benzoicum Acidum

The most marked characteristic pertains to the odor and color of the urine. It has a marked action on metabolism. It produces and cures symptoms of a uric acid diathesis, with urine highly colored and very offensive, and gouty symptoms. Renal insufficiency. Pains suddenly change their locality. Anti-sycotic. Gouty and asthmatic. Urine – changeable color; brown, acid. Enuresis; dribbling, offensive urine of old men. Excess of uric acid. Vesical catarrh from suppressed gonorrhea. Cystitis.

Joints crack on motion. Tearing with stitches. Pain in tendo Achillis. Rheumatic gout; nodes very painful. Gouty deposits. Ganglion; swelling of the wrist. Pain and swelling in knees. Bunion of knee, with severe pain.

Fever. Cold hands, feet, back, knees. Chilliness; cold sweat. Internal heat on awakening. Red spots on skin. Itching in spots.

Berberis Vulgaris

Hepatic, and rheumatic affections, particularly with urinary, hemorrhoidal and menstrual complaints.

Old gouty constitutions. Pain in region of kidneys is most marked, hence its use in renal and vesical troubles, gallstones, and vesical catarrh. It causes inflammation of kidneys with hematuria. Pains may be felt all over body, emanating from small of back. It promotes the flow of bile. Arthritic affections with urinary disturbances. Wandering, radiating pains. Acts well in fleshy persons, good livers, but with little endurance. Spinal irritation. All Berberis pains radiate, are not worse by pressure, but worse in various attitudes, especially standing and active exercise.

Micturition, burning pains. Sensation as if some urine remained after urinating. Urine with thick mucus and bright-red, mealy sediment. Bubbling, sore sensation in kidneys. Pain in bladder region. Pain in the thighs and loins on urinating. Frequent urination: urethra burns when not urinating.

Rheumatic paralytic pain in shoulders, arms, hands and fingers, legs and feet. Neuralgia under fingernails, with swelling of finger-joints. Sensation of cold on outside of thighs. Heels pain. Stitching between metatarsal bones. Pain in heels. Intense weariness and lameness of legs after walking a short distance.

Flat warts. Itching, burning and smarting; worse, scratching; better, cold applications. Small pustules over whole body. Eczema of anus and hands. Circumscribed pigmentation following eczematous inflammation.

Cannabis indica

Urine loaded with slimy mucus. Must strain; dribbling; has to wait some time before the urine flows. Stitches and burning in urethra. Dull pain in region of right kidney.

Palpitation awakes him. Piercing pain, with great oppression. Pulse very slow.

Pain across shoulders and spine; must stoop; cannot walk erect. Thrilling through arms and hands, and from knees down. Entire paralysis of the lower extremities. Pain in soles and calves; sharp pains in knees and ankles; very exhausted after a short walk.

Cantharis

This powerful drug produces a furious disturbance in the urinary and sexual organs, perverting their function, and setting up violent inflammations, and causing a frenzied delirium, simulating hydrophobia symptoms. Puerperal convulsions. Produces most violent inflammation of the whole gastro-intestinal canal, especially lower bowel. Over sensitiveness of all parts. Irritation. Raw, burning pains. Hemorrhages. Intolerable, constant urging to urinate. Gastric, hepatic and abdominal complaints. Gastric derangements of pregnancy. Dysuria. Increases secretion of mucous membranes, tenacious mucus. The inflammations cantharis produces (bladder, kidneys, ovaries, meninges, pleuritic and pericardial membranes) are usually associated with bladder irritation.

Intolerable urging and tenesmus. Nephritis with bloody urine. Violent paroxysms of cutting and burning in whole renal region, with painful urging to urinate; bloody urine, by drops. Intolerable tenesmus; cutting before, during, and after urine. Urine scalds him, and is passed drop by drop. Constant desire to urinate. Membranous scales looking like bran in water. Urine jelly-like, shreddy.

Chelidonium Majus

Polyuria, foaming, yellow urine, like beer dark, turbid. Pain in arms, shoulders, hands, tips of fingers. Icy coldness of tips of fingers; wrists sore, tearing in metacarpal bones. Whole flesh sore to touch. Rheumatic pain in hips and thighs; intolerable pains in heels. Feels paralyzed. Paresis of the lower limbs with rigidity of muscles.

Dry heat of skin; itches, yellow. Painful red pimples and pustules. Old, spreading, offensive ulcers. Wilted skin. Sallow, cold, clammy.

Crotalus horridus

Urinary Organs. Hematuria. Suppression or painful retention of urine. Urine: scanty, dark and red with blood; jelly-like; greenish yellow from much bile; copious and light-colored. Much pain in heart. Palpitation with sore pain in heart; feeling as if heart tumbled over. Pulse hardly perceptible. Phlebitis; varicosis; varicocele. Limbs. Painful paralytic sensation. Rheumatic and neuralgic pains. Bruised pain in joints and bones. Heaviness in limbs. Numb pain as after cramp in anterior of fingers and in toes. Contraction of flexors. Skin. Itching stinging all over; urticaria. Skin dry, stiff like thin parchment; usually cold. Yellow color of whole body (hematic rather than hepatic jaundice). Petechiae. Vesicles; herpes; pimples; boils; carbuncles; burns; stings; pemphigus; ulcers; gangrene; felons; anthrax. Old cicatrices break out again. Peliosis rheumatica. Dropsies.

Cuprum Arsenicum

Kidney failure, excruciating urine, and stained urine. Pain in sacral region, with frequent urging to urinate. Dark red urine; burning pain during and after urination. Strong smelling urine; odor of garlic. Heart’s action weak and hurried, pulse small, compressible, weak, and frequent, though quite regular. Sudden debility, long involuntary inspiration. Empty feeling in stomach, with vertigo and confusion of ideas, and headache between temples. Palpitation of heart, with trembling of limbs. Severer cardiac palpitation. Cardiac chorea (bradycardia): at one time heart beats very irregular and feeble, at another time violent and irregular; attacks appear in paroxysms, action being normal in intervals.

Tremulousness of whole body, very noticeable on attempting to walk. Quivering, impossible to control. Severe prostration.

Body covered with cold moisture, skin dirty pale. Icy coldness of whole body, with cramps and obstinate hiccough. Intermittent, cold clammy sweat.

Cuprum Metallicum

Urgent want to make water, with scant emission. Frequent emission of fetid (dark-red, turbid, with yellowish sediment), viscid urine. Burning shootings in the urethra, during and subsequent to the emission of urine. Bed wetting (nocturia). when a person goes through bed-wetting, extremely watery urine, and feels shooting pain in the urethra.

Spasm of heart. Angina pectoris. Palpitation of the heart. Pulse very changeable; imperceptible; small; soft. Pressive tearing or starting in the limbs. Pain in the joints and in the limbs. Aching in the bones. Rheumatic pains. Shaking pains, which traverse the whole body. Dry eruptions, itch, tetters, with yellow scales. Miliary eruptions. Old ulcers; caries.

Digitalis Purpurea

Pulse – weak, irregular, intermittent, abnormally slow, and dropsy of external and internal parts. Weakness and dilatation of the myocardium. Its greatest indication is in failure of compensation and especially when auricular fibrillation has set in. Slow pulse in recumbent posture, but irregular and dicrotic on sitting up. Auricular flutter and fibrillation especially when subsequent to rheumatic fever. Heart block, very slow pulse. Severe weakness and sinking of strength, faintness, coldness of skin, and irregular respiration; cardiac irritability and ocular troubles after tobacco; jaundice from induration and hypertrophy of the liver. Jaundice with heart disease. Faint.

Cyanosis (bluish appearance). Cardiac muscular failure when asystole is present. Prostration from slight exertion. Collapse. Frequent stitches in heart. Irregular heart especially of mitral disease. Very slow pulse. Intermits; weak. Inequality of pulse. Pericarditis, copious serous exudation. Dilated heart, tired, irregular, with slow and feeble pulse. Hypertrophy with dilatation. Cardiac failure following fevers. Cardiac dropsy.

Continued urging to urinate, in drops, dark, hot, burning, with sharp cutting or throbbing pain at neck of bladder. Suppressed. Ammoniacal, and turbid. Urethritis, phimosis, strangury. Full feeling after urination. Constriction and burning. Brick-dust sediment.

Swelling of the feet. Fingers go to sleep easily. Coldness of hands and feet. Rheumatic pain in joints. Shining, white swelling of joints. Muscular debility. Nocturnal swelling of fingers. Continuous sleepiness.

Fever – sudden flashes of heat, followed by great nervous weakness. Erythema, deep red, worse on back, like measles. Blue distended veins, ears, lips and tongue. Dropsical. Itching and jaundiced.

Helonias Dioica

Diabetes mellitus, and insipidus. Constant aching and tenderness over kidneys. kidney irritation, sickliness, cramps and bluntness. Albuminuria. phosphatic; profuse and clear, urine – saccharine.

Kali Carbonicum

Urinary Organs. Frequent want to urinate, scanty emission of fiery urine. The urine discharged slowly. After micturition prostatitis. Urine pale greenish; turbid. Frequent emission of urine. Incisive pains in bladder. Burning sensation in urethra.

Plumbum Metallicum

The blood, alimentary and nervous systems are the special seats of action of Plumbum. Hemostasis is interfered with, rapid reduction in number of red corpuscles, hence pallor, icterus, anemia. Constrictive sensation in internal organs. Delirium, coma and convulsions. Hypertension and arteriosclerosis. Progressive muscular atrophy. Infantile paralysis. Locomotor ataxia. Excessive and rapid emaciation. Bulbar paralysis. Important in peripheral affections.

The points of attack for Plumbum are the neurexins and the anterior horns. Multiple sclerosis, posterior spinal sclerosis. Contractions and boring pain. All the symptoms of acute. Nephritis with amaurosis and cerebral symptoms. Gout. Urinary – frequent, ineffectual tenesmus. Albuminous; low specific gravity. Chronic interstitial nephritis, with great pain in abdomen. Urine scanty. Tenesmus of bladder. Emission drop by drop. Frequent, ineffectual tenesmus. Albuminous; low specific gravity. Chronic interstitial nephritis, with great pain in abdomen. Urine scanty. Tenesmus of bladder. Emission drop by drop.

Cardiac weakness. Pulse soft and small, dichroitic. Wiry pulse, camp-like constriction of peripheral arteries. Spinal cord sclerosed. Lightning-like pains; temporarily better by pressure. Paralysis of lower extremities. Yellow, dark-brown liver spots. Jaundice. Dry. Dilated veins of forearms and legs.

Paralysis of single muscles, limited movements. Paralysis from overexertion of the extensor muscles in piano players. Pains in muscles of thighs; come in paroxysms. Wrist-drop. Cramps in calves. Stinging and tearing in limbs, also twitching and tingling, numbness, pain or tremor. Paralysis. Feet swollen. Pain in atrophied limbs alternates with colic. Loss of patellar reflex. Hands and feet cold. Pain in knee, sensitive to touch.

Mercurious Coresive

Destroyed secreting portions of kidneys – glomerulonephritis. Intense burning in urethra. Urine hot, burning, scanty or suppressed; bloody, greenish discharge. Albuminous. Tenesmus of bladder. Stabbing pain extending up urethra into bladder, perspiration after urinating. Destroyed kidney function – Glomerular filtration. Albuminuria in early pregnancy.

Terebinthum

Has a selective affinity for bleeding mucous surfaces. Tympanites and urinary symptoms very marked. Inflammation of kidneys, with haemorrhages-dark, passive, fetid. Bright’s disease preceded by dropsy. Drowsiness and strangury. Coma. Urinary strangury, with bloody urine. Scanty, suppressed, odor of violets. Urethritis, with painful erections. Inflamed kidneys following any acute disease. Constant tenesmus. Pulse rapid, small, thready, intermittent.

Acne. Erythema; itching pustular, vesicular eruption; urticaria. Purpura, ecchymosis, dropsies. Scarlatina. Chilblains; with excessive itching and pulsating pains. Aching soreness of the muscles.

Fever with violent thirst, dry tongue, profuse cold, clammy sweat. Typhoid with tympanites, hemorrhages, stupor, delirium. Prostration.

Urea

Constant urging to urinate, beginning at root of penis. Constant urging, with much sediment in urine. From bladder to groins a fatiguing, tearing pain < standing. Profuse diuresis with rapid diminution of dropsy. Albuminuria; bloody urine; general dropsy; intermittent heart. Delirium, nosebleed, urine brown, very albuminous; oedema of pudenda; ascites; pulse small, slow; attacks of suffocation, polyuria; swelling decreased; albumen disappeared. Diabetes; uremia. Urine thin and of low specific gravity. A hydrogogue diuretic in the treatment of dropsies.

Prognosis

The prognosis depends on the cause of TIN, the type (allopathic – takes longer time or Homeopathic – need less time to complete cure) timing of therapy, baseline renal function, prior offending agents, and exposure time to the underlying trigger. Chronicity, such as extensive fibrosis or tubular atrophy, portends worse outcomes. Early identification and removal of the cause improve renal outcomes.

Infectious causes of TIN are usually self-limited and respond well to antimicrobial treatment. Autoimmune-related TIN often relapses depending on the activity of the underlying disease, and renal function should continue to be followed. TINU, in particular, requires close ongoing follow-up with ophthalmology due to its recurrent nature and young cohort. Patients with kidney transplants who experience TIN due to viral causes should have closely monitored immunosuppressant and viral load levels, as each TIN episode can potentially worsen allograft function and precipitate a rejection episode.

Complications

Older patients are more vulnerable to complications. Renal insufficiency is a common manifestation that ultimately progresses to ESRD due to fibrosis of the interstitial and degeneration of tubular epithelial cells. In addition to renal insufficiency, inflammation or infection of proximal tubular cells can result in either decreased synthesis or hypo-responsiveness to erythropoietin by injured cells, leading to reduced RBC production by bone marrow and complications of anemia. TIN also increases angiotensin II activity, which leads to arterial hypertension due to sodium and fluid retention, vasoconstriction, and increased oxidative stress. Increased angiotensin concentration changes the hemodynamic status and oxidative stress, causing vasoconstriction.