Snakebite nephropathy

There is a broad clinical spectrum of renal involvement in snakebite. Besides the local and systemic symptoms, clinical renal manifestations vary from mild proteinuria, haematuria, pigmenturia to acute renal failure. Bites by haemotoxic snakes and myotoxic snakes are the common causes of renal involvement especially acute renal failure. Therefore, renal failure is often associated with haemorrhagic diathesis, intravascular haemolysis and rhabdomyolysis. Renal pathological changes include mesangiolysis, glomerulonephritis, vasculitis, tubular necrosis, interstitial nephritis and cortical necrosis. Tubular necrosis is an important pathological counterpart of acute renal failure. Haemodynamic alterations induced by cytokines and vasoactive mediators leading to renal ischaemia are important in the pathogenesis of acute renal failure. Haemolysis, intravascular coagulation and rhabdomyolysis are important contributing factors. Direct nephrotoxicity can be induced by the venom through metalloproteases and phosphilipase A2. Immunologic mechanism plays a minor role in the pathogenesis of the renal lesion.     

Acute renal failure due to intrinsic renal diseases: review of 1122 cases

In this study we have analyzed incidence, causes and clinical course of ARF due to primary intrarenal disease other than acute tubular necrosis. Thousand hundred and twenty two cases of ARF of diverse etiology were studied over a period of 16 years; July 1984 to Dec, 1999. Surgical ARF 231 (20.6%) were not included in the present study. Intrinsic renal diseases were responsible for ARF in 891 (79.4%) of cases. The most common intrinsic renal diseases 705 (79.4%) causing ARF were ischemic/toxic acute tubular necrosis, but not included in this study. Acute renal failure was related to acute glomerulonephritis (9.3%), acute interstitial nephritis (7%), and renal cortical necrosis in (4.6%) of cases. Therefore intrinsic renal diseases other than ATN were the causative factor for acute renal failure in 186 (20.8%) patients in our study. Crescentic (51.8%) and endocapillary proliferative glomerulonephritis (34.9%), were the main glomerular diseases responsible for ARF and 75.9% of GN was related to infectious etiology. Fifty three percent of acute interstitial nephritis was drug induced and in 25 (40%) patients it was related to an infectious etiology. Renal cortical necrosis due to HUS was observed in 16 (39%) children and majority (76.47%) of the cases had a diarrhoeal prodrome. Obstetrical complications were the main causes (61%) of cortical necrosis in adults with acute renal failure. Thus, intrinsic renal diseases other than ATN were responsible for ARF in 186 (20.8%) cases. Post-infectious glomerulonephritis, acute interstitial nephritis and renal cortical necrosis (complicating HUS in children and obstetrical complications in adult) are the main causes of acute renal failure in our study. Both acute GN and interstitial nephritis had excellent prognosis, however renal cortical necrosis was associated with a very high mortality.     

Unexplained acute renal failure in a toddler: a rare complication of Epstein-Barr virus

A previously healthy toddler developed severe acute renal failure with nephromegaly and peripheral atypical lymphocytosis. Profound interstitial nephritis with acute tubular necrosis was diagnosed by renal biopsy, and both the clinical picture and serological evaluation suggested Epstein-Barr virus (EBV) as the etiological agent. The previous reports of EBV-induced renal failure and the clinical and pathological presentations of interstitial nephritis in children are reviewed.     

Acute renal failure in children with idiopathic nephrotic syndrome

Acute renal failure (ARF) is an uncommon but alarming complication of idiopathic nephrotic syndrome. The renal failure could be secondary to causes evident from the history and evaluation, such as severe intravascular volume depletion, acute tubular necrosis, allergic interstitial nephritis, bilateral renal vein thrombosis, acute pyelonephritis, or rapid progression of the original glomerular disease. It may be termed idiopathic if the underlying cause is undetermined. We present three children with idiopathic nephrotic syndrome who were admitted with acute renal failure. One case was due to drug-induced allergic interstitial nephritis. The other two were idiopathic in nature. Improvement in renal function occurred in the three patients over a variable period of 10 days to 4 weeks. After careful exclusion of well-known causes of acute renal failure, idiopathic acute renal failure (IARF) should be considered as a diagnostic possibility in these patients. The exact pathophysiology of IARF is not understood. Possible proposed explanations include interstitial edema, tubular obstruction, altered glomerular permeability, and unrecognized hypovolemia.     

Acute renal failure from hemoglobinuric and interstitial nephritis secondary to iodine and mefenamic acid

Mefenamic acid ingestion, usually in excess and over prolonged period is known to produce interstitial nephritis, or less commonly papillary necrosis, with acute renal failure. However, it is not dose-dependent for the induction of tubulointerstitial damage. Excess iodine ingestion is known to produce toxicity and possible death, but acute renal failure is rare. There is evidence from clinical and experimental data that iodine has toxic effect on tubular epithelial cells. Iodine has not been documented to produce red cell hemolysis and hemoglobinuria. We present a unique case of acute renal failure from hemoglobinuric and acute interstitial nephritis secondary to suicidal ingestion of potassium iodide solution and also ingestion of a few mefenamic acid tablets. These agents led to potentiation of the renal injury from hemoglobinuric tubulopathy, probably from the iodine, and renal dysfunction from alteration of renal perfusion by selective COX-1 inhibition of prostaglandin production, and induction of acute interstitial nephritis from mefenamic acid, leading to acute renal failure which was reversible by hemodialysis and supportive therapy.     

Acute renal failure in man: pathogenesis in light of new morphological data

The pathogenesis of acute renal failure (ARF) in such common conditions as acute tubular necrosis, acute interstitial nephritis, and primary graft anuria (ischemic transplant ARF) is poorly understood. Animal models may not exactly mimic the situation in man and thus human morphologic studies are of particular importance. Non-replacement of individual sloughed tubular cells and simplification of the brush border and basolateral infoldings of tubular cells are prominent morphologic changes which correlate with the presence of renal failure. It is possible that the initial injury inhibits cell membrane synthesis, thus interfering with proximal tubular sodium reabsorption with resulting activation of the renin angiotensin system and afferent arteriolar vasoconstriction. Tubular backleak, tubular obstruction by casts and debris, and decreased glomerular ultrafiltration coefficient may also play a role. Although poorly studied until now, the renal failure in primary graft anuria may have a completely different pathogenesis from that in acute tubular necrosis and acute interstitial nephritis. Cyclosporine nephrotoxicity is an important component of primary graft anuria, as seen in many transplant centers in the 1980's.     

The spectrum of acute renal failure in IgA nephropathy

Background: Acute renal failure rarely complicates the course of IgA nephropathy. In this study, we have tried to define the mode of presentation, the spectrum of morphology, and the prognostic factors for renal outcome. Methods: Twenty patients with biopsy-proven IgA nephropathy who developed acute renal failure were identified from 2000 to 2009 at a medical center in Taiwan. The patients' records were retrospectively reviewed with respect to clinical presentation, morphology of renal biopsy, and outcomes. Results: On histology, glomerular crescents were present in 11 patients (55%), acute tubular necrosis was identified in 11 patients (55%), acute interstitial nephritis was seen in 4 patients (20%), and extensive tubular red blood cell casts were present in 4 patients (20%). At the end of follow-up, 2 patients (10%) had died, 11 patients (55%) were in remission, and 7 patients (35%) developed end-stage renal disease. The prognostic factors for renal outcome were peak serum creatinine, dialysis support requirement, morphology (prominent glomerular/tubular injury), percentage of glomeruli affected by crescents, and interstitial infiltration (p = 0.04, <0.001, 0.013, 0.05, 0.02, respectively). Conclusions: Our findings suggested that there were four pathogenic mechanisms involved in IgA nephropathy with acute renal failure including (1) crescentic IgA nephropathy; (2) acute tubular necrosis associated with microhematuria and red blood cell casts occluding tubules; (3) acute tubular necrosis not related to microhematuria; and (4) acute interstitial nephritis, apparently induced by drugs. In general, patients with prominent tubular injury had a much higher remission rate than patients with prominent glomerular injury.     

Acute Post Streptococcal Interstitial Nephritis in an Adult and Review of the Literature

While glomerular lesions are a recognized sequel to infection with group A beta haemolytic streptococci, literature on primary tubular lesions, as remote effects of streptococcal infection, is scanty. A case of interstitial nephritis in a 29-year-old woman following streptococcal sore throat is described. This adult admitted with tonsillitis developed acute renal failure from acute interstitial nephritis and subsequently had full recovery of renal function. Acute interstitial nephritis should be included in the differential diagnosis of patients with streptococcal infections who develop acute renal failure.     

Acute Renal Failure Associated with Acute Non-fulminant Hepatitis A: A Case Report and Review of Literature

Most of the cases of non-fulminant hepatitis A carry good renal and overall prognosis. Here we present a case of acute renal failure associated with acute non-fulminant hepatitis A, for which kidney biopsy showed interstitial nephritis and tubular necrosis. We also review the literature and possible pathogenesis.     

Gallium67 scintigraphy in the diagnosis of acute renal disease

67Ga scintigraphy was performed in 44 patients with various biopsy proven forms of renal disease and in a further 64 patients, some with clinically diagnosed renal disease and some with non-renal disorders. Renal uptake of gallium at 48 hours was graded by two blinded observers and by tissue ratios determined by computer. All 11 patients with biopsy proven acute drug-induced interstitial nephritis demonstrated intense, diffuse, bilateral renal 67Ga uptake, a phenomenon observed in only five of the other 30 patients with biopsy proven renal disease and in four of the 64 patients with clinical diagnoses only. No patient with acute tubular necrosis demonstrated significant renal gallium uptake. It is suggested that 67Ga scintigraphy is an excellent screening test for the presence of acute interstitial nephritis and helps to identify which patients with unexplained acute renal failure require renal biopsy.     

Drug-induced granulomatous interstitial nephritis in a pediatric patient

Acute interstitial nephritis (AIN) is a known cause of acute renal failure in children. In most instances, drug therapy is the offending agent. Although granuloma formation has been observed in drug-induced interstitial nephritis, it is not a commonly associated manifestation. This is a case of a 15-year-old white female with Tetralogy of Fallot and pulmonary atresia who developed acute renal failure secondary to drug-induced interstitial nephritis and renal granulomas. In addition to interstitial edema with eosinophils and lymphocytes, her renal biopsy showed interstitial granulomas, immune complexes within tubular basement membranes, and the unusual feature of multinucleated giant cells engulfing tubules. Her acute renal failure resolved after the withdrawal of antibiotics and the initiation of intravenous steroid therapy.     

Granulomatous interstitial nephritis after nonsteroidal anti-inflammatory drugs

Electrolyte and renal hemodynamic imbalance, acute interstitial nephritis with nephrotic-range proteinuria, papillary necrosis, tubular necrosis, and vasculitis are complications after intake of nonsteroidal anti-inflammatory drugs (NSAID). We report on 2 cases of biopsy-proven granulomatous interstitial nephritis with rapidly progressing renal insufficiency. Patient 1 was on ketoprofen for 7 months and indomethacin for 10 weeks before admission to hospital. The medication was not discontinued and renal insufficiency progressed to end-stage renal failure. Renal function did not respond to steroid and tuberculostatic treatment. Patient 2 was on diclofenac for 6 months and indomethacin for 7 weeks before admission to hospital. These drugs were withdrawn at diagnosis and renal function rapidly improved. We conclude that granulomatous interstitial nephritis may be a complication of NSAID medication indicating a cell-mediated immunologic disorder. False diagnosis (sarcoidosis, tuberculosis) may lead to end-stage renal disease (case 1). Discontinuation of medication obviates further therapy (case 2).     

Acute renal failure following multiple wasp stings

We report the cases of two patients who developed acute renal failure following multiple wasp stings. Both patients required dialysis and recovered within 4 weeks. The kidney biopsy from one patient showed acute tubular necrosis with interstitial nephritis. One patient had complete recovery of renal function on follow-up, while the other was lost to follow-up.     

Pantoprazole-induced acute interstitial nephritis

Pantoprazole is a proton-pump inhibitor (PPI) that is commonly prescribed for the treatment of gastroesophageal reflux-related disorders. There are many documented side effects of PPIs. Here we report a case of acute interstitial nephritis, which developed after 6 weeks of treatment with pantoprazole. A 23-year-old man presented with acute renal failure requiring renal replacement therapy. Acute interstitial nephritis was diagnosed by renal biopsy and was successfully treated with corticosteroids and withdrawal of pantoprazole. Drug-induced acute interstitial nephritis can occur with PPIs such as pantoprazole and vigilance needs to be maintained.     

Phenazopyridine associated acute interstitial nephritis and review of literature

Phenazopyridine is a urinary analgesic; commonly seen side-effects of this drug include, orange discoloration of urine, methemoglobinemia, yellowish skin discoloration, hepatitis and acute renal failure. Various case reports with phenazopyridine associated acute renal failure secondary to acute tubular necrosis have been reported in the literature. Acute kidney injury in these patients is caused by either direct injury to renal tubular epithelial cells or secondary to pigment induced nephropathy from hemolytic anemia. Hypoxic injury from phenazopyridine-induced methemoglobinemia has been well documented. We report a case of biopsy proven acute interstitial nephritis, associated with therapeutic doses of phenazopyridine without any evidence of methemoglobinemia or other mechanism of renal injury. Clinicians should be aware of the toxicity of this commonly used drug and should look closely for signs of renal insufficiency. Identifying and stopping the offending medication stays as the first step, but recent studies indicate that early steroid administration improves renal recovery, as well as decreasing the risk of progression to chronic kidney disease with fibrosis and consequent permanent renal damage.     

Late-onset cytomegalovirus-associated interstitial nephritis in a kidney transplant

Cytomegalovirus is the most important viral infection in kidney transplants, but rarely affects the allograft after the sixth month posttransplantation. We present a patient who developed renal failure eighteen months posttransplant; a kidney biopsy showed cytomegalovirus inclusions, acute tubular necrosis and mild interstitial nephritis. After intravenous ganciclovir, renal function transiently improved. Cytomegalovirus pp65 antigen was weekly reported as negative. One month later another biopsy was performed due to renal failure. The findings were consistent with tubular atrophy and severe interstitial nephritis. No cytomegalovirus cellular inclusions were found on histology, including immunohistochemical and polymerase chain reaction studies; pp65 antigen studies were persistently negative. Despite an attempt to recover renal function with steroid therapy, the patient restarted hemodialysis 20 months posttransplantation. This report suggests that cytomegalovirus should be considered as a late cause of kidney failure even in the absence of infection-related symptoms. The irreversible allograft damage can be caused despite the successful eradication of the virus with intravenous ganciclovir.     

Acute tubulointerstitial nephritis after wasp stings

A 61-year-old Caucasian man presented with acute renal failure after multiple wasp stings. The patient required dialysis support temporarily. Work-up failed to show rhabdomyolysis or hemolysis and a kidney biopsy revealed acute allergic interstitial nephritis. The patient's renal function recovered completely after a short course of steroid therapy. Acute renal failure after wasp stings is typically caused by acute tubular necrosis in the setting of hemolysis or rhabdomyolysis. Compared with previously reported cases of acute renal failure associated with bee stings, our patient is unique in that his renal failure was caused by a hypersensitivity reaction apparently to the wasp venom. © 2001 by the National Kidney Foundation, Inc.     

Acute interstitial nephritis of fluindione: about three cases

Acute interstitial nephritis is a frequent cause of acute renal failure, representing about 10% of all biopsied cases. Early recognition of drug-induced acute immunoallergic interstitial nephritis prevents the development of severe chronic renal injury. The list of imputable drugs includes phenindione, a vitamin K antagonist. Fluindione which is also an indanedione derivative is another vitamin K antagonist. We report three biopsy-proved cases of fluindione related acute interstitial nephritis with recovery of renal function after drug withdrawal and prednisone therapy.     

Rabeprazole-induced acute interstitial nephritis

Acute interstitial nephritis is an uncommon but important cause of acute renal failure. Proton pump inhibitors are now thought to be the most common class of drugs implicated in drug-induced acute interstitial nephritis. This is the first reported case of rabeprazole-induced acute interstitial nephritis.     

Interstitial nephritis, acute renal failure in a patient with non-fulminant hepatitis A infection

This is the first report from Norway of a patient with interstitial nephritis and renal failure due to non-fulminant hepatitis A virus (HAV) infection. HAV infection was confirmed by positive anti-HAV IgM serology. All tests for other virus infections were negative. At admittance serum creatinine (s-Creat) and blood urea nitrogen (BUN) concentration were 539 microlmol/l and 32.6 mmol/l increasing the following days to 890 micromol/l and 39.9 mmol/l, respectively. Nine courses of hemodialysis had to be given. Kidney biopsy specimen showed interstitial edema, lymphocytic cell infiltration and acute tubular injury with normal glomeruli. Examination with immunohistochemistry was negative. In contrast to the findings associated with HBV and HCV infection in which glomerular disease is predominantly found, the HAV infection in our patient was associated with interstitial nephritis and acute tubular necrosis. The prognosis of the renal failure due to HAV infection was good although the recovery was substantially delayed.