Wasp envenomation-induced acute renal failure: a report of three cases

Acute renal failure is an unusual complication of wasp stings. We report three cases who developed acute renal failure after multiple wasp stings (Vespa magnifica). Two patients had evidence of intravascular haemolysis and rhabdomyolysis whereas one patient investigation showed no evidence of intravascular haemolysis or rhabdomyolysis. All three cases had impaired liver functions. Oligo-anuria was seen in all three of the patients and all of them required dialytic support. One patient died of massive gastrointestinal bleeding while the remaining two recovered completely. Although acute renal failure after wasp stings is typically caused by acute tubular necrosis in the setting of haemolysis or rhabdomyolysis, in some patients, renal failure may result from a direct nephrotoxic effect or acute interstitial nephritis from a hypersensitivity reaction to the wasp venom.     

Rhabdomyolysis and acute renal failure in children

Acute renal failure (ARF) is an important complication of rhabdomyolysis. However, the contributing factors to the development of ARF in children with rhabdomyolysis remain obscure. The aim of this study was to clarify the factors contributing to the development of ARF in children with rhabdomyolysis. This is a retrospective review of the clinical characteristics, laboratory data, pediatric risk of mortality (PRISM) scores, the occurrence of systemic inflammatory response syndrome (SIRS) criteria, and the number of dysfunctional organs in 18 children with rhabdomyolysis seen in our hospital between 1991 and 2000. The patients were divided into an ARF group (n=9) and a non-ARF group (n=9). All patients with ARF had more than two dysfunctional organs. The incidence of dehydration, serum concentrations of myoglobin, creatinine kinase, aspartate aminotransferase, and lactate dehydrogenase, PRISM scores, and the numbers of SIRS criteria and dysfunctional organs were higher in the ARF group than the non-ARF group. The blood pH and base excess, and urinary pH were lower in the ARF group than in the non-ARF group. These results suggest that ARF is more likely to develop in the presence of dehydration, metabolic acidosis, or severe muscle damage, or with multiple organ failure in children with acute rhabdomyolysis. Received: 12 April 2001 / Revised: 20 August 2001 / Accepted: 21 August 2001     

Renal tubular calcification in six nephrotic children with acute renal insufficiency

Summary: A review of 42 primary nephrotic children who underwent kidney biopsies found that six patients had calcification of the renal tubules (aged 2-9 years). These six patients showed significant increases in weight gain, blood pressure, urinary protein, serum urea nitrogen and urinary calcium/creatinine, and significant decreases in serum phosphate, % tubular reabsorption of phosphate and creatinine clearance as compared with 36 nephrotic patients without tubular calcification. Furthermore, these patients received high dose furosemide, and five of six patients received methylprednisolone pulse therapy to treat progressive renal dysfunction. the interval before the first kidney biopsy and after both the onset of the nephrotic syndrome, and the start of glucocorticoid therapy, including methylprednisolone pulse therapy and furosemide, ranged from 1 to 5 months excluding one patient (33 months). Although one patient received haemodialysis, renal insufficiency was resolved from 10 to 18 days after its onset. Glucocorticoid therapy, including methylprednisolone pulse therapy and high dose furosemide in primary nephrotic children with acute renal insufficiency, induced calcification of the renal tubules.     

Risks of acute renal failure after cardiopulmonary bypass surgery in children: a retrospective 10-year case-control study

To our knowledge there are no case-control studies that haveexamined the main risk factors for acute renal failure (ARF)following cardiopulmonary bypass surgery in children. We thereforeevaluated the potential risk factors in a large retrospectivecase-control study. Sixty-one of 2262 children (2.7%) developedpostcardiopulmonary bypass surgery ARF requiring peritonealdialysis (PD) from 1982 to 1991. Fifty-eight of 61 cases (medianage 8.5 months) were selected by systematic sampling and matchedwith 176 controls who did not develop ARF. The four matchingvariables were age, cardiopulmonary bypass and circulatory arrestduration, and year of operation. Mortality rate was 79% in cases (controls: 18%). Forty-threeof 48 of the deceased cases did not recover renal function;no renal cause of death was found; 13 of 61 cases survived andrecovered renal function. Multiple regression analysis showedthe following significant risk factors for postcardiopulmonarybypass surgery ARF: central venous hypertension >12 h (oddsratio (OR) 9.6); systolic arterial hypotension >12 h (OR8.9); dopamine dosage >15 µg/kg/min (OR 3.0); adrenaline(OR 5.9) and isoproterenol (OR 13.5) use. High preoperativeserum creatinine, cyanosis, and vasodilator use were not significantrisk factors. We conclude that: (1) haemodynamic alterations were the maincause of postcardiopulmonary bypass surgery ARF; (2) ARF wasassociated with but was not the cause of the high mortalityrate; (3) the risk of ARF increased almost 10-fold after 12h of central venous hypertension and/or of systolic arterialhypotension; (4) effective dosages of inotropes might have beena risk factor for ARF; (5) a slight precardiopulmonary bypasssurgery reduction of renal function alone did not representan increased risk for ARF.     

Urinary enzymes in acute renal failure

Intestinal-type alkaline phosphatase (IAP) has been localizedto the S3 segment of the renal tubule in previous studies, asite believed to be particularly vulnerable to toxic and ischaemicdamage. During a 17-month period a pilot study of the valueof urinary enzyme measurements (IAP and tissue non-specificalkaline phosphatase—TNAP, using monoclonal antibody-basedimmunoassays, and N-acetyl-beta-glucosaminidase—NAG, usingcolorometric assay) in 50 prospectively followed cases of acuterenal failure (ARF) was performed. Urinary enzymes were measuredat initial evaluation (‘start’), and then each dayfor 14 days, with the highest enzyme value (‘peak’)also used for analysis. Patients were divided into prerenal(n=16), renal (n=28), postrenal (n=6) categories according tostandard criteria. Of the renal ARF patients 23 of 28 had acutetubular necrosis (ATN), 3 of 28 acute interstitial nephritis(AIN), and 2 of 28 acute glomerulonephritis (AGN); 18 of 50had a fatal outcome and 1 of 50 was dialysis-dependent at discharge(‘poor’ prognosis group), while 31 of 50 survivedhospital without becoming dialysis-dependent (‘good’prognosis group). Median enzyme concentration were increased in ‘poor’compared to ‘good’ prognosis patients: start IAP3.2 versus 2.2 U/g creat (NS), start NAG 48.6 versus 13.7 (P<0.01),start TNAP 3.5 versus 0.9 (P<0.02). When renal ARF patientsalone were analysed, only IAP (3.2 versus 1.3 U/g creat at start)and NAG (57.9 versus 7.8 U/g creat at start) were significantlyincreased in the poor compared to the good prognosis group.Peak values showed similar trends. Of all patients, five witha start IAP>12 U/g creat died, and all survivors had a startIAP<12, but 14 of 19 poor prognosis patients also had a startIAP<12. All urinary enzymes were less in the postrenal group,but only the IAP significantly so. None of the enzymes weresignificantly different between prerenal and renal ARF groups. Urinary enzymes IAP, NAG, TNAP appear to be unhelpful in determiningthe site of renal injury in ARF, except for postrenal cases,where IAP was significantly lower. There were too few patientswith AGN or AIN to test the hypothesis that the enzymes wouldbe less in glomerular compared to tubular pathologies. Despitea low sensitivity, the start IAP may be a marker of outcomein ARF if the high positive predictive value for death is confirmedin larger studies.     

Acyclovir-induced acute renal failure

SUMMARY: Acyclovir is an effective antiviral agent in the treatment of herpes simplex and varicella-zoster viral infections. the best known side-effects of this drug are significant nephrotoxicity and neurotoxicity. We report on a diabetic patient with acute retinal necrosis who developed non-oliguric acute renal failure during the administration of high doses of intravenous acyclovir (500 mg/m² intravenous infusion every 8h). No obvious uremic symptoms or signs were noted. No obvious haematuria, proteinuria or crystalluria were noted in the urine. After discontinuing the acyclovir administration, renal function partially recovered. In this paper, we also review the mechanism of acyclovir-induced acute renal failure, and the precipitating factor of acyclovir-induced acute renal failure. Finally, we must once again emphasize the importance of hydration and routine check ups for renal function in preventing acyclovir-induced acute renal failure.     

Chronic renal failure due to granulomatous interstitial nephritis in sarcoidosis: Response to corticosteroid therapy

Chronic renal failure due to granulomatous interstitial nephritis in sarcoidosis is a rare phenomenon, and its response to corticosteroid therapy is not well known. We report a patient with sarcoidosis who presented with chronic renal failure and hypercalcemia, but who did not exhibit nephrocalcinosis. Renal histology findings showed the presence of noncaseating granuloma and heavy interstitial nephritis. Although hypercalcemia was remarkably improved by corticosteroid therapy, chronic renal failure, due to interstitial fibrosis and scarring, remained unchanged. This case reinforces evidence supporting the effectiveness of corticosteroid therapy in granulomatous interstitial nephritis of sarcoidosis, and suggests the need for early initiation of the therapy to avoid permanent renal dysfunction.     

Prognosis of severe drug-induced acute interstitial nephritis requiring renal replacement therapy

ObjectiveDrug-induced acute interstitial nephritis (DAIN) is often associated with improved outcomes, whereas some patients may still progress to chronic kidney disease (CKD). The aim of this study was to evaluate the prognosis of patients with severe DAIN requiring renal replacement therapy (RRT) at baseline, and to explore the risk factors of progression to CKD.MethodsWe performed a retrospective study of patients with severe DAIN confirmed by renal biopsies in our center over a 10 years period, all the patients received RRT at presentation. The clinical and pathological characteristics at baseline were recorded, and the outcomes (renal function recovered or progressed to CKD) during follow-ups were also evaluated. Univariate and multivariate logistic regression analysis were performed to identify the independent risk factors of progression to CKD.ResultsSeventy-two patients who met the inclusion criteria were enrolled, 13 patients (18.0%) progressed to CKD (GFR < 60 ml/min/1.73 m²) after at least 6 months of follow-up, the remaining 59 patients achieved a favorable renal function recovery. Compared with patients who achieved renal function recovery (recovery group), the patients progressed to CKD (progression group) were older and had longer interval from symptom onset to treatment with steroids. The peak serum cystatin C concentration was higher in progression group than recovery group. Higher score of interstitial fibrosis/tubular atrophy (IFTA) and more interstitial inflammatory cells infiltration were detected in renal tissue in progression group. According to multivariable analysis, higher peak cystatin C concentration (OR = 2.443, 95% CI 1.257, 4.746, p = 0.008), longer interval to treatment with corticosteroids (OR = 1.183, 95% CI 1.035, 1.352, p = 0.014) were independent risk factors of progression to CKD. The cutoff value of cystatin C concentration was 4.34 mg/L, at which the sensitivity and specificity were 76.9% and 89.3%, respectively; the cutoff value of interval to treatment with corticosteroids was 22.5 days, at which the sensitivity and specificity were 81.8% and 79.5%, respectively.ConclusionRenal function was reversible in majority of patients with severe DAIN requiring RRT when early identification and treatment. Higher peak cystatin C concentration and longer interval to treatment with corticosteroids associated with worse renal prognosis.     

Cause of death in acute renal failure.

The cause of 636 deaths during acute renal failure (ARF) occurring between 1956 and 1989 were analysed. Deaths due to haemorrhage and to non-recovery of renal function have declined but cardiovascular deaths and withdrawal of active treatment have increased. The causes of death varied with the clinical situation in which ARF arose. The most important factor contributing to death was the underlying cause of ARF. 67% deaths due to sepsis resulted from infection present at the time of development of ARF. Deaths due to secondary complications have declined, indicating that the precipitating causes of ARF are the main determinant of overall mortality.     

Continuous arteriovenous hemofiltration in acute renal failure

This extensive review describes the settings for continuous arteriovenous hemofiltration (CAVH) and attempts to compare it to traditional dialysis therapies for acute renal failure. In addition hemodynamic stability, membrane biocompatibility, nutrition, fluid and solute removal, operational characteristics, anticoagulation, replacement solutions, drug removal, complications, and trouble shooting during CAVH are all discussed in detail. The cost of CAVH v dialysis is equal. CAVH is probably the renal replacement therapy of choice for hemodynamically unstable patients with acute renal failure and contraindications to peritoneal dialysis.     

Rifampicin-associated acute renal failure and hemolysis: a rather uncommon but severe complication

Abstract

Rifampicin is a widely used anti-tuberculosis agent. Apart from hepatotoxicity, rifampicin can rarely lead to adverse reactions of immunologic nature such as acute renal failure (ARF). We report the case of 57-year-old previously healthy man under treatment for pulmonary tuberculosis who presented with hemolysis and severe ARF. Rifampicin was discontinued and the patient was treated with fluid repletion, iv furosemide and dialysis therapy. Kidney biopsy revealed acute tubulointerstitial nephritis with no evidence of granulomas. The patient significantly improved and was discharged after 51 days of hospitalization. Clinicians using rifampicin should be aware of this rather uncommon but severe complication.     

Kinetics of carbamylated haemoglobin in acute renal failure.

BACKGROUND: Carbamylation of proteins by isocyanic acid, the reactive form of cyanate derived from urea, is increased in uraemia and may contribute to uraemic toxicity. Kinetics of carbamylation that may reflect uraemic toxicity is not clearly defined in acute renal failure (ARF). METHODS: Twenty-eight patients with ARF and 13 with chronic renal failure (CRF) were included in the study in order to determine changes in carbamylated haemoglobin concentration (CarHb) in ARF. The usefulness of this parameter for differentiating ARF from CRF was also investigated. CarHb was measured by high-performance liquid chromatography after acid hydrolysis. RESULTS: Mean CarHb level (expressed as microg carbamyl valine per gram (CV/g) Hb) was significantly higher in ARF (54.3+/-5.2) than in normal subjects (31.6+/-1.3). On admission, CarHb level was correlated with duration of ARF prior to hospitalization in the intensive care unit (r(2)=0.723, P<0.001). CarHb was significantly higher at recovery in the subgroup of patients requiring haemodialysis than in the subgroup not requiring haemodialysis (82. 4+/-11.3 vs 46.7+/-5.2, P<0.01). Similarly dialysis patients lost more weight (8.6+/-1.4 vs 2.7+/-0.5 kg, P<0.005) and had higher averaged blood urea levels in the 20 days prior to recovery (17. 6+/-1.9 vs 11.3+/-1.8 mol/l, P<0.05). After recovery, CarHb level decreased at a rate of 0.219 microg CV/g Hb per day in patients with reversible renal insufficiency. CarHb concentration was higher in patients with CRF. A cut-off CarHb value of 100 microg CV/g Hb had a sensitivity of 94% and a positive predictive value of 94% for differentiating ARF from CRF. CONCLUSIONS: Kinetics of CarHb showed a near normal red blood cell life span in ARF. Changes in CarHb enabled, with a good sensitivity, the distinction to be made between patients who recovered from ARF and those with sustained renal impairment, whether due to prior CRF or resulting from parenchymal sequelae. Measurement of CarHb is valuable at clinical presentation of ARF in patients with an unknown medical history of renal disease.     

Reversible renal failure and nephrotic syndrome without interstitial nephritis from zomepirac

This report describes two patients with the clinical syndrome of reversible renal failure and nephrotic syndrome caused by the nonsteroidal anti-inflammatory agent, zomepirac sodium. What is unique about this report are the pathologic findings on renal biopsy which showed fusion of foot processes consistent with minimal change disease without evidence of an interstitial infiltrate. A cause-and-effect relationship of the disease to zomepirac administration is strongly suggested by the resolution of the renal dysfunction when the drug was stopped and by more than eighteen months of follow-up without evidence of any impairment in renal function.     

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.     

Metformin lactic acidosis, acute renal failure and rofecoxib

A patient with acute renal failure associated with lactic acidosisas a result of concurrent treatment with metformin is described.Rofecoxib may have been a precipitating factor. The risk ofrenal failure with the use of traditional NSAIDs is well known.However, what is less well appreciated is the role that theCOX 2 inhibitors may play in the development of renal failurewhich, when it occurs in a patient on metformin, can lead toa potentially disastrous outcome. Br J Anaesth 2003; 91: 909–10     

Malignant pleural mesothelioma with associated minimal change disease and acute renal failure

Paraneoplastic manifestations in malignant pleural mesothelioma are rare. We report a case of malignant pleural mesothelioma associated with minimal change disease (MCD). A 58-year-old man with occupational exposure to asbestos presented with severe peripheral edema, heavy proteinuria, and acute renal failure shortly after the diagnosis of mesothelioma had been confirmed. The renal biopsy demonstrated MCD. The underlying pathogenesis of this association remains unknown.