Oliguric Renal Failure and Acute Tubular Necrosis

1963 ◽  
Vol 47 (4) ◽  
pp. 1023-1042 ◽  
Author(s):  
Miles H. Sigler
2019 ◽  
Vol 5 (6) ◽  
pp. 220-223
Author(s):  
Tarkeswar Aich ◽  

Introduction: The involvement of the kidney in falciparum malaria has been known for decades. In 1944, Spitz observed acute renal failure due to falciparum infection in soldiers during World War II. This observation was later supported by other workers who detected oliguria developing in patients with black water fever. The initial clinical pattern is that of reversible renal dysfunction or pre-renal azotemia, which rapidly progresses to acute tubular necrosis if treatment is not started early. Patients with malaria induced renal failure are hypercatabolic with blood urea and serum creatinine levels rising rapidly.Oliguric as well non-oliguric renal failure are observed and duration of oliguric renal failure ranges from a few days to several weeks depending on the severity of renal dysfunction. Acute renal failure in falciparum malaria is usually associated either with acute intravascular haemolysis or heavy parasitemia. Acute renal failure in falciparum malaria is also observed in patients with severe intravascular haemolysis resulting in haemoglobinuria. It may be induced by malarial fever or by anti-malarial drugs in a patient with or without G6-PD deficiency. Materials and Methods: This is a hospital based cross sectional study carried out in a total of 50 cases of acute renal failure who were selected from diagnosed patients of P. falciparum malaria. Cases were confirmed either by P. falciparum antigen test and/or peripheral blood smear test(both thick and thin smear).Malarial ARF (MARF) is diagnosed when serum creatinine level > 3 mg/dl, and/or urine output < 400 ml/24hrs despite adequate rehydration. Result: Out of 174 cases of falciparum malaria 50 patients (28.7%) had acute renal failure in falciparum malaria. 36 (72%) cases were males and 14 (28%) were females, indicating a much higher incidence in males. Approximately 78% of the cases in the present study were below the age of 40 years. The youngest was 15 years old and the oldest was 61 years old (Mean age – 32 ± 11.6 years). All were febrile (100%) and a majority had oliguria or anuria (72%); jaundice was detected in 30 (60%) patients on presentation. Hepatomegaly & Splenomegaly were found in 76% & 66% of the cases respectively. Out of the total 50 cases of malaria induced ARF, 14 cases (28%) had pre-renal ARF while in the majority, 72% the clinical course was that of ATN. The pathogenesis of ATN in the 36 cases was found to be heavy parasitaemia in 40% of the cases, IV hemolysis with haemoglobinuria in 3 (6%) of cases; and cholestatic jaundice in 26% of falciparum patients. Examination of the urinary sediments revealed that albumin was present in urine in 40 cases (80%). Majority of the patients had significant rise in blood urea level with a mean value of 177 mg. S. creatinine levels ranged between 3.2 - 13.6 mg with a mean value of 7.83 mg. The mean creatinine clearance rate was 11.71 ml/min. The overall mortality rate was 26%. Conclusion: AKI is common in Falciparum malaria. The pathogenesis of AKI is largely unknown but may be related to the erythrocyte sequestration and agglutination within the renal microcirculation interfering with flow and metabolism. Clinically and pathologically, this syndrome manifests as Pre-renal azotemia and acute tubular necrosis. Acute renal failure may occur simultaneously with other vital-organ dysfunction (in which case the mortality risk is high) or may progress as other disease manifestations resolve. Early dialysis or hemofiltration considerably enhances the likelihood of a patient’s survival, particularly in acute hypercatabolic renal failure. Severity of oliguria and presence of one or more associated complications like pulmonary oedema, acidosis, and altered sensorium have considerable influence on the outcome of the patients.


1992 ◽  
Vol 3 (3) ◽  
pp. 688-697
Author(s):  
Sara Douglas

Acute tubular necrosis (ATN) is the most common cause of acute renal failure. Early recognition of patients who are at risk for ATN can prevent or improve the course of ATN. Acute renal failure is classified as prerenal, intrinsic, or postrenal disease. ATN is classified as a type of intrinsic renal disease. The clinical course of ATN is divided into the renal failure phase, diuretic phase, and recovery phase, with each phase having distinct symptoms and laboratory findings. Diagnosis of ATN often is complicated and confusing; understanding of laboratory findings can facilitate the critical care nurse’s ability to assess those at risk for ATN. The care and treatment of the patient with ATN is complicated, and specific treatments are discussed in detail. The critical care nurse can play a vital role in identifying the patient at risk, preventing the development of ATN in those at risk, and providing appropriate care for those who develop ATN


1972 ◽  
Vol 1 (1) ◽  
pp. 65-69 ◽  
Author(s):  
J. M. Hayes

Acute renal failure has oliguria and uraemia as its cardinal manifestations. The syndrome may be due to acute tubular necrosis, glomerulonephritis, urinary tract obstruction and occlusive vascular disease. The renal damage due to acute tubular necrosis is of uncertain aetiology. Renal cortical ischaemia and depression of glomerular filtration rate are important in the pathogenesis. Activation of the renin-angiotensin system and glomerular coagulation may prove to be important in these changes. The differentiation between reversible oliguria and established renal failure is generally accomplished on clinical grounds and the response to a therapeutic trial of mannitol. Measurement of urinary sodium concentration and osmolality are valuable adjuncts. The keystone of management is the prevention of symptomatic uraemia. Infection and haemorrhage have now replaced pulmonary oedema and hyperkalaemia as the major causes of death. The mortality rate remains high in acute tubular necrosis and a significant mortality occurs in the diuretic phase.


Renal Failure ◽  
1992 ◽  
Vol 14 (4) ◽  
pp. 533-539 ◽  
Author(s):  
Helga Maria Mazzarolo-Cruz ◽  
Décio de Oliveira Penna ◽  
Luis Balthazar Saldanha ◽  
Elza Hissako Kanashiro ◽  
Jenner Cruz ◽  
...  

2011 ◽  
Vol 1 (2) ◽  
pp. 33-35
Author(s):  
Rana A. Nabalawi

Background: Heat induced illnesses are variable from a mild heat exhaustion to a severe heat stroke and its systemic complications. Millions of pilgrims annually perform the Islamic obligatory mission of Hajj, are vulnerable to heat induced illnesses, especially when Hajj falls in the summer period. This is a retrospective study of the renal and electrolyte abnormalities in heat stroke patients during Hajj. Method: We selected randomly 472 patients out of 2044 patients diagnosed as heat stroke over 5 years from 1986-1991 for this study. The diagnosis of heat stroke was based on: 1) Rectal temperature > 40°C, 2) Hot dry skin and 3) Neurological deficit presenting as delirium, coma with or without convulsions. The renal function and electrolytes of all these patients were obtained. Results: All the 472 patients revealed significant electrolyte abnormalities: hypophasphatemia 98% (P + 0.55 ± 0.05 mmol/L), hyponatremia Na+ 70% (128 + 1 mmol/L), hypocalcemia 70% (Ca + 2.01 ± 0.02 mmol/L), hypokalemia 32% (K+3.3 ± 01 mmol/L), and hypomagnesaemia (Mg 0.06 ± 0.01 mmol/L) in 30%. Metabolic acidosis and compensatory respiratory alkalosis was seen in most patients. Acute renal failure that required dialysis developed in 180 (8.8%) patients. In 100 patients, the most common cause was Rhabdomyolysis (68%). The rest had ischemic acute tubular necrosis (32%) with a mortality of 15% compared to 20% in all the 472 patients. The risk mortality was higher in patients with a temperature of 42°C, comatose at presentation and older than 50 years. Conclusion: During Hajj, electrolyte abnormalities in heat stroke were found to be fairly common. Acute renal failure was mainly due to Rhabdomyolysis, which carry better prognosis compared to other causes of acute tubular necrosis.


1995 ◽  
Vol 5 (9) ◽  
pp. 1647-1652
Author(s):  
G R Johnson ◽  
S F Wen

The binge drinking of alcohol combined with the ingestion of a nonsteroidal anti-inflammatory drug (NSAID) is a recently described cause of reversible acute renal failure. The pathogenetic mechanisms leading to acute tubular necrosis in this setting include the initial compromise in renal perfusion due to alcohol-induced extracellular volume contraction and the superimposed renal hemodynamic alterations induced by the NSAID that interfere with the renal autoregulation. Although alcohol may also cause rhabdomyolysis leading to acute tubular necrosis, this is usually not apparent in these cases. Previously, only three such cases have been reported but the incidence is likely to be higher in view of the prevalence of alcohol and NSAID use. Herein is presented another patient in whom the features of flank pain and acute renal failure in association with binge drinking and NSAID ingestion constitute a characteristic syndrome.


2000 ◽  
Vol 278 (5) ◽  
pp. H1555-H1564 ◽  
Author(s):  
Linda C. Clark ◽  
Hanan Farghaly ◽  
Sabiha R. Saba ◽  
David L. Vesely

Seventeen Sprague-Dawley rats had ischemic nonoliguric acute renal failure (ARF) induced by vascular clamping resulting in their preischemic blood urea nitrogen (BUN) and creatinine levels of 16 ± 1 and 0.56 ± 0.05 mg/dl to increase to 162 ± 4 and 8.17 ± 0.5 mg/dl, P < 0.001, respectively, at day 4 of postischemia. Vessel dilator, a 37-amino-acid cardiac peptide hormone (0.3 μg ⋅ kg− 1 ⋅ min− 1ip), decreased the BUN and creatinine levels to 53 ± 17 mg/dl and 0.98 ± 0.12 mg/dl ( P < 0.001) in another seven animals where ARF had been established for 2 days. Water excretion doubled with ARF and was further augmented by vessel dilator. Transthoracic echocardiography revealed left ventricular dilation as a probable cause of the increase in vessel dilator in the circulation with ARF, and vessel dilator infusion reversed this dilation. At day 6 of ARF, mortality decreased to 14% with vessel dilator from 88% without vessel dilator. Acute tubular necrosis was <5% in the vessel dilator-treated rats compared with 25% to >75% in the placebo-treated ARF animals. We conclude that vessel dilator improves acute tubular necrosis and renal function in established ARF.


Medicine ◽  
1989 ◽  
Vol 68 (3) ◽  
pp. 173 ◽  
Author(s):  
STEEN OLSEN ◽  
JAMES F. BURDICK ◽  
PAUL A. KEOWN ◽  
A. C. WALLACE ◽  
LORRAINE C. RACUSEN ◽  
...  

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