scholarly journals P. falciparum Malaria induced Renal impairment

2019 ◽  
Vol 5 (6) ◽  
pp. 220-223
Author(s):  
Tarkeswar Aich ◽  
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Serum Creatinine ◽  
Renal Dysfunction ◽  
Falciparum Malaria ◽  
Acute Tubular Necrosis ◽  
Mean Value ◽  
Intravascular Haemolysis ◽  
Tubular Necrosis ◽  
Oliguric Renal Failure

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.

scholarly journals Incidence of Acute Renal Failure in Full Term Neonates with Birth Asphyxia

2019 ◽  
Vol 4 (1) ◽  
pp. 671-674
Author(s):  
Chandra Bhushan Jha ◽  
Akhil Tamrakar
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Serum Creatinine ◽  
Renal Injury ◽  
Urine Output ◽  
Birth Asphyxia ◽  
Full Term ◽  
Acute Renal Injury ◽  
Term Neonates ◽  
Oliguric Renal Failure

Introduction: Birth asphyxia is an eventuality having far reaching consequences in the neonatal period. Hypoxia and ischemia can cause damage to almost every tissue and organ in the body and various target organs involved. Renal insult is a recognized complication of birth asphyxia and carries a poor prognosis. Timely detection of renal dysfunction and appropriate management may favorably alter the prognosis in many neonates with birth asphyxia. Objective: The present study was done to find out the incidence of acute renal failure in the full term neonates with birth asphyxia. Methodology: A cross sectional study was conducted at Birat Medical College Teaching Hospital, Morang, Nepal from 1st September 2017 to 28th February 2018. Fifty full term neonates born with Apgar score of <6 at 5 minutes and fulfilling inclusion criteria were enrolled in the study. Asphyxiated neonates having Serum creatinine >1.5gm/dl or urine output<1ml/kg/hr were labeled as cases of Acute Renal Failure. Blood sample for serum creatinine was collected at 24hrs, 48 hrs and 72 hrs of life. Results A total of 50 term asphyxiated neonates were enrolled in the present study. Among them 54% and 46% were males and females respectively with male to female ratio of 1.2:1. In the present study 62% of cases developed acute renal failure in either of the first three days of life with mean urine output 1.02±0.27ml/kg/hr and mean serum creatinine of 1.49±0.32 mg/dL. The incidence of oliguric renal failure was 52% and non oliguric renal failure was 48%.The association between serum creatinine and urine output was statistically significant. Conclusion: In the present study birth asphyxia has been an important cause of neonatal acute renal injury, revealing 31 (62%) cases. Monitoring urine output and serum creatinine has helped in detecting the asphyxiated neonates with acute renal injury in the early stage.

Acute Tubular Necrosis: Diagnosis, Treatment, and Nursing Implications

1992 ◽  
Vol 3 (3) ◽  
pp. 688-697
Author(s):  
Sara Douglas
Keyword(s):  
At Risk ◽  
Renal Failure ◽  
Acute Renal Failure ◽  
Critical Care ◽  
Acute Tubular Necrosis ◽  
Early Recognition ◽  
Recovery Phase ◽  
Vital Role ◽  
Laboratory Findings ◽  
Tubular Necrosis

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

scholarly journals Management of Acute Renal Failure

1972 ◽  
Vol 1 (1) ◽  
pp. 65-69 ◽  
Author(s):  
J. M. Hayes
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Acute Tubular Necrosis ◽  
Urinary Tract Obstruction ◽  
Renin Angiotensin System ◽  
Sodium Concentration ◽  
Therapeutic Trial ◽  
Angiotensin System ◽  
Tubular Necrosis ◽  
Occlusive Vascular Disease

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.

IgA Nephropathy: Acute Renal Failure, Acute Tubular Necrosis, and Features of Postinfectious Acute Glomerulonephritis

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 ◽  
...  
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Iga Nephropathy ◽  
Acute Tubular Necrosis ◽  
Acute Glomerulonephritis ◽  
Tubular Necrosis

scholarly journals NEPHROTOXICITY ATTRIBUTED TO MEGLUMINE ANTIMONIATE (GLUCANTIME) IN THE TREATMENT OF GENERALIZED CUTANEOUS LEISHMANIASIS

1999 ◽  
Vol 41 (1) ◽  
pp. 33-37 ◽  
Author(s):  
M.L.O. RODRIGUES ◽  
R.S. COSTA ◽  
C.S. SOUZA ◽  
N.T. FOSS ◽  
A.M.F. ROSELINO
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Side Effects ◽  
Serum Creatinine ◽  
Cutaneous Leishmaniasis ◽  
Urine Osmolarity ◽  
Hepatic Enzyme ◽  
Meglumine Antimoniate ◽  
Tubular Necrosis ◽  
Electrocardiographic Abnormalities

Background: Pentavalent antimonials have became of basic importance for the treatment of leishmaniasis. Their most severe side effects have been reported to be increased hepatic enzyme levels and electrocardiographic abnormalities. Nephrotoxicity has been rarely related. Observations: We report a case of generalized cutaneous leishmaniasis involving a 50-year old male patient who was submitted to treatment with meglumine antimoniate (Glucantime). He developed acute renal failure (ARF) due to acute tubular necrosis (ATN), followed by death after receiving a total of 53 ampoules of Glucantime. Conclusions: The treatment with Glucantime was responsible by ARF diagnosed in this patient. The previous urine osmolarity and serum creatinine levels were normal and the autopsy showed ATN. It should be pointed out if ARF may also be explained by massive deposits of immunocomplexes by leishmania antibodies and antigens due to the antigenic break by the antimonial compound, since our patient presented countless lesions covering the entire tegument, similar to the Hexheimer phenomenon, but at the autopsy no glomerular alterations were seen.

scholarly journals Renal and Electrolyte Abnormalities in Heat Stroke during Hajj

2011 ◽  
Vol 1 (2) ◽  
pp. 33-35
Author(s):  
Rana A. Nabalawi
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Acute Tubular Necrosis ◽  
Heat Stroke ◽  
Respiratory Alkalosis ◽  
Summer Period ◽  
Dry Skin ◽  
Systemic Complications ◽  
Tubular Necrosis ◽  
Electrolyte Abnormalities

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.

scholarly journals Syndrome of flank pain and acute renal failure after binge drinking and nonsteroidal anti-inflammatory drug ingestion.

1995 ◽  
Vol 5 (9) ◽  
pp. 1647-1652
Author(s):  
G R Johnson ◽  
S F Wen
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Binge Drinking ◽  
Acute Tubular Necrosis ◽  
Extracellular Volume ◽  
Renal Perfusion ◽  
Flank Pain ◽  
Inflammatory Drug ◽  
Tubular Necrosis ◽  
Anti Inflammatory

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.

Contrast-induced nephropathy (Pharmacology of X-ray contrast agents)

2016 ◽  
Vol 7 (1) ◽  
pp. 97-105 ◽  
Author(s):  
Vladislava A Raptanova ◽  
Alexandra A Speranskaya ◽  
Sergei N Proshin
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Serum Creatinine ◽  
Renal Dysfunction ◽  
Urine Volume ◽  
Contrast Induced Nephropathy ◽  
Acute Renal Dysfunction ◽  
X Ray ◽  
Sustained Reduction ◽  
Nephrotoxic Drugs

In the last 30 years the use of X-ray contrast media (RCM) has increased significantly during urography, angiography, computed tomography, and operating procedures. Every year the world uses about 60 million doses of PKM, but, despite the use of newer and less nephrotoxic drugs, the risk of contrast-induced nephropathy (CIN) is still significant, especially among patients with prior renal impairment. Contrast induced nephropathy is a major cause of acute renal injury and is a huge problema in clinical practice. So far, con-tradictions remain in the understanding of many aspects of CIN. Contrast-induced nephropathy is acute renal failure (ARF) occurs within 48-72 hours after intravenous administration of contrast sub-stances. Toxicity PKC determined their molecular structure and its ability to dissociate in aqueous solution into ions which consist of salts which dissociate into cations and anions. The contrast-induced nephropathy is manifested in the increase of serum creatinine of 44 mmol/L (0.5 mg / dl) or more and the same rise in serum creatinine of more than 25 % compared to baseline in the absence of other possible causes. ARF is a sudden and sustained reduction in glomerular filtration rate and urine volume, or both together. Thus renal dysfunction existing even more than 1 month can be regarded as acute renal dysfunction. Usually the development of acute renal failure occurs within 1-7 days. The criteria of sustainability is a dysfunction of its registration within 24 hours or more. The aim: to consider different approaches to the pathogenesis, risk factors and achievements in the prevention of contrast-induced nephropathy.

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