Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0028961 (oliguria)
 1,847 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In rats, single intravenous doses of folic acid induce damage to renal tubular epithelium, deposition of folic acid in tubular lumens, increase in wet kidney weight, oliguria and interstitial connective tissue proliferation. Separation of the nephrotoxic and obstructive effects of folic acid was attempted by pretreatment with NH4Cl or NaHCO3. These effects of folic acid were unaltered by pretreatment with NH4Cl and there was, in addition, accumulation of eosinophilic droplets in papillary collecting duct epithelium. After pretreatment with NaHCO3, folic acid deposition is decreased or absent; there is a smaller increase in wet kidney weight; the rats are polyuric rather than oliguric; interstitial connective tissue proliferation is reduced; and no droplets form in papillary collecting ducts, but lesions are still present in proximal convoluted tubule epithelial cells. These findings indicate that folic acid has direct nephrotoxic effects independent of intraluminal folic acid deposition, and that damage to renal epithelium, unlike that induced by many nephrotoxins, occurs at several levels of the nephron.
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PMID:Experimental folic acid nephropathy. 284 Jun 27

The sequence in which the various therapies discussed above are instituted can be viewed as a continuum that parallels the severity of the underlying cirrhotic state (Figure 6). In the earliest stages of the disease urinary sodium excretion is plentiful and negative salt balance can be achieved by simply lowering dietary sodium intake. As the disease advances neurohumoral effectors become more activated initially resulting in more intense renal salt retention and later in a progressive decline in renal function. Eventually, the filtered load of sodium becomes completely reabsorbed by the tubule and the final urine becomes virtually devoid of salt. If some component of the filtered load reaches the collecting duct or beyond, spironolactone will be effective in increasing urinary sodium excretion. Once sodium reabsorption is complete, proximal to the collecting duct, then thiazides and later loop diuretics will have to be added to spironolactone to increase urinary sodium excretion. Eventually, the filtered load is completely reabsorbed proximal to the thick ascending limb of Henle. At this point the patient is resistant to the effects of diuretics and requires more invasive procedures such as repetitive large volume paracentesis to remain in salt balance. In the terminal stages of the disease the glomerular filtration rate falls to such a degree that oliguria, azotemia, and eventually uremia are present and the patient is clinically diagnosed with hepatorenal syndrome. Vasoconstrictive input focused on the kidney is severe and irreversible. Renal failure is functional in nature; however, restoration of near normal renal function can be obtained following a liver transplant.
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PMID:Pathogenesis of ascites and renal salt retention in cirrhosis. 1036 77

There has been a progressive increase in the number of intensive care patients being transferred to nephrology units because of improper dosage of drugs, especially patients with chronic kidney disease (CKD). Voriconazole is a new synthetic triazole derivative with stronger therapeutic activity against fungal infections than fluconazole or itraconazole. Its effectiveness is associated with high nephrotoxicity, affecting patients with CKD in particular. The adverse effects of voriconazole involve several segments of the nephron, particularly the proximal tubule, medullary thick ascending limb, and collecting duct, causing loss of potassium and magnesium and backdiffusion of hydrogen ions. We report the case of an 86-year-old man with moderate CKD who developed acute renal failure as a result of inadequate dosage of voriconazole. He developed oliguria, electrolyte imbalance and fluid overload requiring hemodialysis. Vericonazole withdrawal associated with short daily hemodialysis treatment led to the recovery of diuresis, kidney function, and electrolyte balance. In conclusion, in elderly patients with liver disease and moderate CKD, thorough evaluation is needed before the administration of voriconazole in order to establish the most appropriate dose.
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PMID:[Voriconazole compromises renal function in an elderly CDK patient with Candida albicans infection]. 2054 25

The distal tubule and collecting duct in kidney regulate water homeostasis. TMOD1 is an actin capping protein that plays an important role in controlling the organization of actin filaments. In this study, we found TMOD1 was specifically expressed in distal tubules and collecting ducts. To investigate the role of TMOD1, we created Tmod1flox/flox mice and bred them with Ksp-Cre mice to generate tubule-specific Tmod1 knockout mice, Tmod1flox/flox/Ksp-Cre+ (designated as TFK). As compared with control mice, TFK mice showed oliguria, hyperosmolality urine, and high blood pressure. To determine the mechanisms underlying this phenotype, we performed label-free quantitative proteomics on kidneys of TFK and control mice. Total of 83 proteins were found differentially expressed. Bioinformatic analysis indicated that biological processes, including protein phosphorylation and metabolic process, were involved in TMOD1 regulatory network. Gene set enrichment analysis showed that multiple pathways, such as phosphatidylinositol signaling system and GnRH signaling pathway, were strongly associated with Tmod1 knockout. Western blot validated the down-regulation of three proteins, TGFBR2, SLC25A11, and MTFP1, in kidneys of TFK mice. Our study provides valuable information on the molecular functions and the regulatory network of Tmod1 gene in kidney, as well as the new mechanisms for the regulation of water balance.
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PMID:Quantitative proteomics reveals TMOD1-related proteins associated with water balance regulation. 3133 16