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Fulltext Acute renal failure in falciparum malaria

Segasothy M, Swaminathan M, Kong NC

Med J Malaysia, 1994 Dec;49(4):412-5.
PMID: 7674979

We report two patients who had cerebral malaria, heavy parasitemia, hyperbilirubinemia, hypercatabolism with rapid rises of blood urea and serum creatinine and acute renal failure. There was no evidence of intravascular hemolysis. Renal biopsy was consistent with acute tubular necrosis. Both patients responded to treatment with intravenous quinine and dialysis.

Matched MeSH terms: Kidney Tubular Necrosis, Acute/etiology; Kidney Tubular Necrosis, Acute/pathology
Effects of pre and post-treatments with dipyridamole in gentamicin-induced acute nephrotoxicity in the rat

Balakumar P, WitnessKoe WE, Gan YS, JemayPuah SM, Kuganesswari S, Prajapati SK, et al.

Regul Toxicol Pharmacol, 2017 Mar;84:35-44.
PMID: 27993652 DOI: 10.1016/j.yrtph.2016.12.007

This study investigated the pretreatment and post-treatment effects of dipyridamole (20 mg/kg/day, p.o.) in gentamicin-induced acute nephrotoxicity in rats. Rats were administered gentamicin (100 mg/kg/day, i.p.) for 8 days. Gentamicin-administered rats exhibited renal structural and functional changes as assessed in terms of a significant increase in serum creatinine and urea and kidney weight to body weight ratio as compared to normal rats. Renal histopathological studies revealed a marked incidence of acute tubular necrosis in gentamicin-administered rats. These renal structural and functional abnormalities in gentamicin-administered rats were accompanied with elevated serum uric acid level, and renal inflammation as assessed in terms of decrease in interleukin-10 levels. Dipyridamole pretreatment in gentamicin-administered rats afforded a noticeable renoprotection by markedly preventing renal structural and functional abnormalities, renal inflammation and serum uric acid elevation. On the other hand, dipyridamole post-treatment did not significantly prevent uric acid elevation and renal inflammation, and resulted in comparatively less protection on renal function although it markedly reduced the incidence of tubular necrosis. In conclusion, uric acid elevation and renal inflammation could play key roles in gentamicin-nephrotoxicity. Dipyridamole pretreatment markedly prevented gentamicin-induced acute nephrotoxicity, while its post-treatment resulted in comparatively less renal functional protection.

Matched MeSH terms: Kidney Tubular Necrosis, Acute/blood; Kidney Tubular Necrosis, Acute/chemically induced; Kidney Tubular Necrosis, Acute/drug therapy*; Kidney Tubular Necrosis, Acute/prevention & control*
Acute renal failure following multiple wasp stings

Thiruventhiran T, Goh BL, Leong CL, Cheah PL, Looi LM, Tan SY

Nephrol Dial Transplant, 1999 Jan;14(1):214-7.
PMID: 10052513
Matched MeSH terms: Kidney Tubular Necrosis, Acute/etiology; Kidney Tubular Necrosis, Acute/pathology
Fulltext A case of acute kidney injury by near-drowning

Amir A, Lee YL

Malays Fam Physician, 2013;8(3):34-6.
PMID: 25893056 MyJurnal

Acute kidney injury following immersion or near-drowning is rarely described and no data from Malaysia have been found. We report a case of acute kidney injury following a near-drowning event. A 20-year-old man who recovered from near-drowning in a swimming pool 5 days earlier presented to our clinic with abdominal pain, anorexia, nausea and polyuria. Dipstick urinalysis showed a trace of blood. The serum creatinine level was 10-fold higher than the normal range. A bedside ultrasound showed features suggestive of acute tubular necrosis. He is then referred to the hospital with the diagnosis of acute kidney injury with the possibility of acute tubular necrosis secondary to near-drowning. We suggest that any patient presenting after immersion or near-drowning to be should assessed for potential acute kidney injury.

Matched MeSH terms: Kidney Tubular Necrosis, Acute
Fulltext Sub-chronic toxicological evaluation of cleistanthin A and cleistanthin B from the leaves of Cleistanthus collinus (Roxb.)

Parasuraman S, Raveendran R, Rajesh NG, Nandhakumar S

Toxicol Rep, 2014;1:596-611.
PMID: 28962273 DOI: 10.1016/j.toxrep.2014.08.006

OBJECTIVE: To investigate the toxicological effects of cleistanthin A and cleistanthin B using sub-chronic toxicity testing in rodents.
METHOD: Cleistanthins A and B were isolated from the leaves of Cleistanthus collinus. Both the compounds were administered orally for 90 days at the concentration of 12.5, 25 and 50 mg/kg, and the effects on blood pressure, biochemical parameters and histology were assessed. The dose for sub-chronic toxicology was determined by fixed dose method according to OECD guidelines.
RESULT: Sub-chronic toxicity study of cleistanthins A and B spanning over 90 days at the dose levels of 12.5, 25 and 50 mg/kg (once daily, per oral) revealed a significant dose dependant toxic effect in lungs. The compounds did not have any effect on the growth of the rats. The food and water intake of the animals were also not affected by both cleistanthins A and B. Both the compounds did not have any significant effect on liver and renal markers. The histopathological analysis of both cleistanthins A and B showed dose dependent morphological changes in the brain, heart, lung, liver and kidney. When compared to cleistanthin A, cleistanthin B had more toxic effect in Wistar rats. Both the compounds have produced a dose dependent increase of corpora amylacea in brain and induced acute tubular necrosis in kidneys. In addition, cleistanthin B caused spotty necrosis of liver in higher doses.
CONCLUSION: The present study concludes that both cleistanthin A and cleistanthin B exert severe toxic effects on lungs, brain, liver, heart and kidneys. They do not cause any significant pathological change in the reproductive system; neither do they induce neurodegenerative changes in brain. When compared to cleistanthin A, cleistanthin B is more toxic in rats.

Matched MeSH terms: Kidney Tubular Necrosis, Acute