Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0033687 (proteinuria)
 24,015 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In a study performed in Tamale, in the Northern region of Ghana, cystatin C, a new and sensitive indicator of the glomerular filtration rate (GFR), was used to estimate the frequency of renal dysfunction in 78 children with uncomplicated, Plasmodium falciparum malaria. The excretion in urine of albumin, immunoglobulin G and alpha1-microglobulin was also investigated. Plasma concentrations of cystatin C were found to be elevated in 17% of the children, indicating subclinical impairment of renal function. As most (85%) of the children had glomerular as well as tubular patterns of proteinuria, it appears that both glomerulonephritis and damage to tubular cells often occur in P. falciparum malaria.
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PMID:Renal dysfunction in children with uncomplicated, Plasmodium falciparum malaria in Tamale, Ghana. 1283 20

Malaria is a major public health problem in tropical countries. About 500 million people suffer from malaria, leading to death in 1 to 3 million cases. Acute kidney injury (AKI) is one of the most dreaded complications of severe malaria. As per World Health Organization criteria, acute renal failure (serum creatinine level, > or =3 mg/dL or > or =265 micromol/L) occurs as a complication of Plasmodium falciparum malaria in less than 1% of cases, but the mortality rate in these cases may be up to 45%. It is more common in adults than children. Renal involvement varies from mild proteinuria to severe azotemia associated with metabolic acidosis. It may be oliguric or nonoliguric. AKI may be present as a component of multi-organ dysfunction or as a lone complication. The prognosis in the latter is generally better. Several pathogenic mechanisms interplay for the clinical manifestation. The predominant lesions are acute tubular necrosis and mild proliferative glomerulonephropathy. These patients do not progress to chronic kidney disease. The management of malaria-induced AKI includes appropriate antimalarials (parenteral artesunate or quinine), fluid electrolyte management, and renal replacement therapy at the earliest. The use of diuretics should be avoided.
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PMID:Malaria and acute kidney injury. 1862 Sep 62

Glomerulonephritis occurs as a rare form of renal manifestation in Plasmodium falciparum malaria. Herein, we report a case of falciparum malaria-associated IgA nephropathy for the first time. A 49-yr old male who had been to East Africa was diagnosed with Plasmodium falciparum malaria. Microhematuria and proteinuria along with acute kidney injury developed during the course of the disease. Kidney biopsy showed mesangial proliferation and IgA deposits with tubulointerstitial inflammation. Laboratory tests after recovery from malaria showed disappearance of urinary abnormalities and normalization of kidney function. Our findings suggest that malaria infection might be associated with IgA nephropathy.
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PMID:Immunoglobulin A nephropathy associated with Plasmodium falciparum malaria. 2246 11

Malaria is a parasitic infection of global importance but has a high prevalence in the developing countries. Renal failure is a common complication of severe Plasmodium falciparum malaria and has been reported in up to 40% of all cases. Acute kidney injury (AKI), however, is not commonly associated with Plasmodium vivax infection. In those patients who develop AKI following P. vivax infection, the cause is commonly attributed to mixed undiagnosed falciparum infection or coexistent sepsis, dehydration, or hypotension. Infrequently, an association of P. vivax infection with thrombotic microangiopathy (TMA) has been reported. The purpose of this report is to describe renal failure due to TMA following malaria caused by P. vivax. A 24-year-old female presented with a history of fever and jaundice of two weeks duration followed by progressive oliguria and swelling of the face and feet five days after the onset of fever. The evaluation revealed normal blood pressure, anemia, thrombocytopenia, azotemia, unconjugated hyperbilirubinemia with mildly elevated transaminases, and elevated lactate dehydrogenase. Peripheral smear was positive for P. vivax, and schistocytes were seen. She was given intravenous artesunate followed by oral primaquine for 14 days. Urine examination showed proteinuria and microscopic hematuria. She remained oliguric and dialysis dependent, and her kidney biopsy revealed patchy cortical necrosis involving 40% of sampled cortex with widespread fibrinoid necrosis of the vessel wall, red blood cell fragmentation, and luminal thrombotic occlusion. Hemodialysis was discontinued after three weeks when there was the improvement of renal function over time, and her serum creatinine decreased to 2.2 mg/dL by six weeks. Patients with P. vivax malaria developing renal failure may have TMA. Renal biopsy, if performed early in the course of the disease, may identify TMA and institution of plasma exchange in such patients could help in early recovery.
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PMID:Acute kidney injury due to acute cortical necrosis following vivax malaria. 3146 55