Rapid onset of co-trimoxazole induced interstitial nephritis

An infant developed anuric renal failure within 18 hours of starting therapy with Co-trimoxazole for otitis media. There was no prior exposure to Co-trimoxazole, sulfonamides or trimethoprim. A renal biopsy revealed acute interstitial nephritis with eosinophilic infiltration (AIN). The lymphocyte blast transformation test revealed increased proliferation of the patient's lymphocytes on exposure to Co-trimoxazole (Bactrim). Both parents have clinically demonstrated hypersensitivity to sulfonamides. The extremely short latent period between ingestion of the offending drug and the onset of AIN in the absence of prior exposure to the drug has been reported previously. It suggests that drug induced AIN may develop more rapidly in patients with a strong genetic hypersensitivity to the drug.     

Acute interstitial nephritis in childhood

Three children aged 11 to 14 years with acute interstitial nephritis (AIN) are presented. In one patient AIN developed following antibiotic treatment with trimethoprim/sulfamethoxazole (TMP/SMX). In two patients no infection, drug, or toxin could be implicated. Severe polyuric renal failure without elevation of blood pressure was the predominant clinical feature. Uveitis occurred either simultaneously with the nephritic symptoms or several weeks after complete recovery of renal function. Renal functions were characteristically altered and led to suspicion of AIN even prior to renal biopsy. Renal plasma flow was relatively more reduced than glomerular filtration rate (GFR) with an accordingly increased filtration fraction. Quantitative evaluation of selective tubular functions revealed significant transport deficiencies for glucose, amino acids, inorganic phosphate and low molecular weight proteins. In two patients GFR increased rapidly following initiation of steroid treatment and tubular symptoms simultaneously disappeared. In one patient spontaneous remission occurred. We conclude that—in contrast to adults—the prognosis of AIN in childhood is favorable. Although general clinical features are rather nonspecific, symptoms of decreased tubular reabsorption ability provide a good indication of the diagnosis and may contribute to enhanced recognition of this disease.     

Future strategies in the treatment of acute renal failure: growth factors, stem cells, and other novel therapies

PURPOSE OF REVIEW: Acute renal failure remains a significant cause of morbidity and mortality in adults and children. Despite advances in understanding the pathophysiology of acute renal failure, little progress has been made in its treatment. This review assesses the recent data on current and promising new therapies for acute renal failure. RECENT FINDINGS: The first section of the review describes the recent therapies that have been used in humans, all of whom have been adults. The second section evaluates the use of agents given in experimental animal models during or after the onset of acute renal failure. The third section describes the many animal studies using therapies before the onset of experimental renal failure. The final section discusses how the emerging field of stem cell research might be used to treat acute renal failure. SUMMARY: Among the recent studies in humans, the most intriguing have been the use of atrial natriuretic peptide in patients with nonoliguric renal failure and isotonic sodium bicarbonate infusions to prevent radiocontrast medium-induced renal failure. Among the agents used in animal studies, those with the greatest potential were hepatocyte growth factor and ethyl pyruvate, because they seem to protect against or accelerate recovery from acute renal failure after the renal insult. Finally, stem cell therapy may someday offer the best option for recovery from acute renal failure.     

Acute renal failure

Acute renal failure is characterized by an increase in the blood concentration of creatinine and nitrogenous waste products and by the inability of the kidney to appropriately regulate fluid and electrolyte homeostasis. There are many different causes of acute renal failure in children, including prerenal disease, intrinsic renal failure, which includes ischemic hypoxic insults, and obstructive uropathy. This review will focus on hypoxic/ischemic acute renal failure, the most common causes of hospital acquired acute renal failure in children. This review will briefly discuss the epidemiology and incidence of acute renal failure in pediatric patients and review new insights into the pathogenesis of acute renal failure. including hemodynamic alterations induced by alterations in nitric oxide and endothelin metabolism, the role of the inflammatory response, and alteration in polarity in the acute renal failure. The therapy of acute renal failure has changed substantially during the past few years. Controlled trials (in adults) to test the efficacy of "renal dose" dopamine have shown that it is ineffective, and hemofiltration has become increasingly popular as a choice of therapy for acute renal failure.     

Acute reversible kidney failure in IgA nephritis

Four patients with acute renal failure during an acute course of IGA-nephritis are described. Percutaneous renal biopsies showed only minor glomerular lesions in all patients. Immunosuppressive therapy was not necessary. In all patients acute renal failure was completely reversible. The four patient showed further episodes of macrohematuria without acute renal failure. All patients had normal renal function, normotensive blood pressure and microhematuria during interval. In three of the patients we found erythrocytes casts and a mild protein excretion. IGA-nephritis is one of the most common types of glomerulonephritis in adolescents and adults. If acute renal failure occurs during a course of IGA-nephritis with macroscopic haematuria a percutaneous renal biopsy has to be performed. Only in case of severe crescents formation (greater than 75%) immunosuppressive therapy is necessary. Glomerular lesions are responsible for long time prognosis.     

Potential risk factors for the development of acute renal failure in preterm newborn infants: a case-control study

AIMS: To determine in a case-control study possible associations between the development of acute renal failure in preterm newborns and therapeutic interventions, particularly drug treatments. METHODS: The study population was 172 preterm infants of <38 weeks gestation; 71 had acute renal failure and 101 were controls closely matched for gestational age and birth weight. Maternal and neonatal information was collected for both groups through questionnaires and interviews. Routine data on renal variables were also collected. Univariate and multivariate logistic regression analyses were performed. RESULTS: Very low birthweight infants were at high risk of acute renal failure (79% of cases were <1500 g). However, the acute renal failure was transient. Mothers of infants with acute renal failure received more drugs during pregnancy and delivery (mainly antibiotics and non-steroidal anti-inflammatory drugs). Of the possible therapeutic interventions, intubation, catheterisation, and phototherapy were mainly applied to case subjects. A low Apgar score and patent ductus arteriosus were diagnosed in a greater percentage of neonates with acute renal failure. Moreover, in the first few days of life and before diagnosis of acute renal failure, case subjects received more drugs (antibiotics, non-steroidal anti-inflammatory drugs, and diuretics) and for a longer time. In the multivariate logistic analysis, medullary hyperechogenicity (odds ratio (OR) 4.491; 95% confidence interval (CI) 1.879 to 10.731) and ceftazidime administration (OR 5.082; 95% CI 1.493 to 17.297) were associated with a greater risk of acute renal failure. CONCLUSIONS: The results suggest the need for careful monitoring of very low birthweight infants and attention to drug treatments, as it is difficult to differentiate between normality and renal failure in the first few days of life.     

Acute heart failure and acute renal failure in Kawasaki disease

Acute renal failure and acute heart failure are rare in Kawasaki disease. We experienced two patients with Kawasaki disease who presented acute renal failure and acute heart failure. These two patients gave us an important insight into the understanding of water balance and fluid therapy in Kawasaki disease. One patient showed acute prerenal failure due to fluid exudation from the intravascular to the extravascular space, and subsequent acute heart failure. The other patient showed acute heart failure caused by fluid infusion for the treatment of dehydration. It is suggested that acute renal failure could be caused by a fluid shift from the intravascular to the extravascular space in Kawasaki disease. It is also demonstrated that the reserve of cardiac function could be decreased in patients with Kawasaki disease due to myocarditis even with normal echocardiography and chest X-rays.     

Hypercalcaemia-induced acute renal failure as a presenting feature of T-cell leukaemia

A 14-year-old patient presented with hypercalcaemia-induced acute renal failure. Investigation yielded a diagnosis of T-cell leukaemia. Chemotherapy resulted in complete remission, a return of serum calcium levels to normal and consequent improvement of renal function.Abbreviations ARF acute renal failure - PTH parathormone     

Acute renal failure after exercise in a child with renal hypouricemia

We describe a 15 year old boy with renal hypouricemia who developed acute renal failure after a school athletics meeting, accompanied by appendicitis. During acute renal failure, the highest level of uric acid was 5.0 mg/dL, creatinine 7.9 mg/dL and urea nitrogen 58.6 mg/dL. After recovery, the serum uric acid fell to 0.9 mg/dL and the fractional excretion of uric acid (FEu_A) exceeded the normal range. The probenecid and pyrazinamide tests showed that the patient had a total defect of uric acid reabsorption. This case suggested that strenuous exercise could be responsible for acute renal failure in patients with renal hypouricemia.     

Treatment of renal failure in neonates.

Thirty neonates with acute renal failure were studied, 27 of whom died (90%) including nine of 12 treated by peritoneal dialysis. Three main aetiological groups were identified. Septicaemia was a principal cause of late onset acute renal failure, with an incidence equal to that of serious perinatal disorders. It is recommended that tolazoline should be used with caution in the treatment of hyperkalaemia as it may have a role in the aetiology of acute renal failure, the incidence of which is increasing.     

Doppler evaluation of renal blood flow velocity as a predictive index of acute renal failure in perinatal asphyxia

Aim of our study was to evaluate Doppler renal blood flow velocity in asphyxiated neonates and to correlate renal function to Doppler findings. Doppler renal blood flow velocity was evaluated in 23 severely asphyxiated neonates born at a gestational age >32 weeks and compared to our standard Doppler data obtained in 25 healthy neonates comparable for gestational age and birth weight. Renal Doppler ultrasound was performed on the 1st and 3rd days of life. Renal function was investigated in the first 2 weeks of life. Asphyxiated neonates showed mean values of systolic velocity and mean velocity significantly reduced (P< 0.001) compared with our standard Doppler values on the 1st day of life. Seven out of the 23 asphyxiated neonates were affected by acute renal failure and 14 showed no renal involvement. Two neonates were oliguric but did not develop acute renal failure. On the 1st day of life, neonates with acute renal failure had significantly lower mean values of systolic velocity and mean velocity than the asphyxiated neonates without renal involvement (P< 0.01). All 7 neonates affected by acute renal failure showed a systolic velocity more than 2SD below the mean standard value, while only 4 of the 16 asphyxiated neonates (25%) without acute renal failure had low systolic velocity values on the 1st day of life. Doppler velocities in asphyxiated neonates were similar to standard values on the 3rd day of life. Renal failure recovered before the 11th day of life in all cases. Conclusion Our findings indicate that decreased Doppler renal flow systolic velocity observed in asphyxiated neonates on the 1st day of life is a useful predictive index for subsequent development of acute renal failure, with 100% sensitivity and 63.6% specificity. Received: 21 July 1997 / Accepted in revised form: 24 November 1997     

Free oxygen radicals in acute renal failure

OBJECTIVE: To assess the levels of free oxygen radicals in acute renal failure and their predictive value in clinical outcome. DESIGN: Prospective. SETTING: Intensive care unit. METHODS: Study was conducted in 50 children (25 with acute renal failure and 25 age and sex matched controls). Blood urea, serum creatinine, serum protein, uric acid and free oxygen radical markers were estimated in both groups. Superoxide dismutase (SOD), glutathione peroxidase(GPx) and lipid peroxide (LPO) were estimated in blood by standard techniques. RESULTS: Hemolytic uremic syndrome (HUS) was a major cause of acute renal failure (52%), rest were due to acute glomerulonephritis (AGN), septicemia and renal venous thrombosis. In the renal failure group 56% of the patients were dialyzed (peritoneal) and the mortality was 28% (7/25). The levels of SOD, GPx and LPO were significantly raised in renal failure group. Higher values of LPO, SOD and GPx were documented in subjects who expired. The most important independent variable for predicting clinical outcome was LPO with a sensitivity of 89.4%, specificity of 93%, positive predictive value of 95%. CONCLUSION: Levels of free oxygen radicals (SOD, LPO and GPx) are raised in acute renal failure and these enzymes can be used as marker of renal injury. LPO levels are highly sensitivity and specific for predicting the clinical outcome     

Prognostic factors in neonatal acute renal failure

Sixteen infants, 2 to 35 days of age, had acute renal failure, a diagnosis based on serum creatinine concentrations greater than 1.5 mg/dL for at least 24 hours. Eight infants were oliguric (urine flow less than 1.0 mL/kg/h) whereas the remainder were nonoliguric. To determine clinical parameters useful in prognosis, urine flow rate, duration of anuria, peak serum creatinine, urea (BUN) concentration, and nuclide uptake by scintigraphy were correlated with recovery. Nine infants had acute renal failure secondary to perinatal asphyxia, three had acute renal failure as a result of congenital cardiovascular disease, and four had major renal anomalies. Four oliguric patients died: three of renal failure and one of heart failure. All nonoliguric infants survived with mean follow-up serum creatinine concentration of 0.8 +/- 0.5 (SD) mg/dL whereas that of oliguric survivors was 0.6 +/- 0.3 mg/dL. Peak serum creatinine concentration did not differ between those patients who were dying and those recovering. All infants who were dying remained anuric at least four days and revealed no renal uptake of nuclide. Eleven survivors were anuric three days or less, and renal perfusion was detectable by scintigraphy in each case. However, the remaining survivor (with bilateral renal vein thrombosis) recovered after 15 days of anuria despite nonvisualization of kidneys by scintigraphy. In neonates with ischemic acute renal failure, lack of oliguria and the presence of identifiable renal uptake of nuclide suggest a favorable prognosis.     

Pathogenesis and treatment of acute renal failure

This article reviews the current understanding of the pathophysiologic sequence of events that culminate in an acute renal insult. The use of urinary indices to differentiate the physiologic causes of oliguria, namely, diminished intravascular volume or renal perfusion, from an established acute renal failure, is discussed for children and adolescents, as well as for neonates. Treatment modalities for the support of children with acute renal failure are described in detail.     

Urinary sediment in acute renal failure

Over a one-year period, 31 episodes of acute renal failure in children have been studied for urine sediment by contrast phase microscopy (maintained diuresis: 15, oligoanuria: 16, dialysed patients: 9). The etiologies of acute renal failure were: sepsis = 8; nephrotoxicity = 7; hemolytic uremic syndrome = 5; acute nephritic syndrome = 3; hemodynamical changes = 4; obstructive renal failure = 2; others = 3; acute rejections after renal allograft were excluded. The first urine sediment examination was performed 5 days after the onset of renal failure, and has been controlled in 11 children. In 28 cases (90%), there was a good correlation between clinical, biological, ultrasonographic and pathological (4 cases) data. The mechanism of renal failure has been determined by urine sediment examination in most cases, sometimes allowing to rectify a previous diagnosis. The value of this examination seems to be more of anatomoclinical than of prognostic interest, mainly for definite (hemolytic uremic syndrome) or polyfactorial (oncohematological diseases) renal dysfunctions.     

Indian Carp (Labeo Rohita) Gall Bladder Poisoning-Report of Four Cases in a Single Family

The ingestion of Indian carp gallbladder may result in transient hepatitis with subsequent acute renal failure. This case series also illustrates the importance of understanding the use and potential serious complications of alternative medicines. So fish gallbladder poisoning should be considered in unexplained acute renal failure in Chinese and Asian patients. We report four family members who developed acute renal failure and toxic hepatitis at the same time following ingestion of raw Indian carp (Labeo rohita) gall bladder.     

Unusual cause of acute renal failure in infancy

Acute renal failure due to intratubular obstruction is uncommon in infants. Two infants presenting with acute renal failure associated with acute gastroenteritis were found to have bilateral global nephrocalcinosis secondary to oxalosis.     

Reflux nephropathy complicated by acute post-streptococcal glomerulonephritis

A 7 years old male with severe bilateral vesicoureteral reflux developed acute renal failure without evidence of either infection or obstruction. The diagnosis of acute post-streptococcal glomerulonephritis was confirmed by clinical, serological and histological evaluation. The patient's creatinine clearance decreased from 25 ml/min/1.73 m2 to 10-13 ml/min/1.73 m2 following the acute nephritic episode and chronic dialysis therapy was required thereafter. This patient illustrates that a glomerular etiology should be suspected when acute renal failure occurs in a patient with reflux nephropathy and suggests that the prognosis of acute post-streptococcal glomerulonephritis may be worse in children with pre-existing renal disease.     

Acute renal failure as the initial manifestation of systemic lupus erythematosus in children

In two patients with systemic lupus erythematosus, acute renal failure was the initial manifestation. The diagnosis was eventually established on the basis of serologic tests and characteristic renal histopathologic findings. We emphasize the need to consider systemic lupus erythematosus as a cause of acute renal failure of glomerular origin, because appropriate therapy may alter the outcome of the disease.