Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0032617 (polyuria)
 3,056 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 66-year-old Japanese man presented with persistent hyponatremia without polydipsia and polyuria. Laboratory examination showed serum sodium of 117 mEq/l, plasma osmolality 239 mosm/kg, urine sodium 108 mEq/l, urine osmolality 577 mosm/kg, and normal levels (less than 2.0 pg/ml) of serum antidiuretic hormone (ADH). ADH release was regulated normally with changes in plasma osmolality. No obvious cause for the syndrome of inappropriate secretion of ADH (SIADH) could be detected. However, 20 months later, the patient had bouts of hematuria and was found to have cancer of the urinary bladder. Increased renal sensitivity to ADH was suspected as the underlying mechanism of SIADH.
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PMID:A case of syndrome of inappropriate secretion of antidiuretic hormone (SIADH) with low plasma concentrations of antidiuretic hormone. 160 Feb 74

We report a 41-year-old man with bladder cancer who developed polyuria following successful treatment of hypercalcemia and who was found to have a transitional cell carcinoma within the pituitary gland at autopsy. He also had widespread bone metastases. Although primary urogenital cancers rarely metastasize to the pituitary, the patient's clinical course led us to suspect metastatic disease from the bladder cancer. Metastasis to the pituitary gland is more common than generally thought and should be considered in patients with advanced cancer who develop polyuria and polydipsia.
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PMID:Diabetes insipidus due to pituitary metastasis from bladder cancer. 205 38

In the present investigation, administration of a single i.p. dose of the anticancer drug merbarone [5-(N-phenylcarboxamido)-2-thiobarbituric acid] produced an acute and reversible decrease in renal function in female but not male Fischer 344 rats. The renal lesion in female rats was biochemically characterized as a decrease in p-aminohippuric acid accumulation by renal slices along with polyuria, glucosuria, proteinuria, and enzymuria. These functional changes were accompanied by histopathologic changes of focal tubular necrosis that was confined to the deep cortex and outer stripe of the outer medulla. The changes in these parameters were dose-dependent and were observed at doses as low as 0.2 x MELD(10) (12 mg/kg). This low merbarone dose increased urinary glucose and protein excretion by 26- and 9-fold, respectively, in the initial 16-h urine collection in female rats. This increase was accompanied by a 2- to 15-fold increase in the excretion of N-acetyl-beta-D-glucosaminidase (NAG), gamma-glutamyl transpeptidase (gamma-GTP), and lactate dehydrogenase (LDH) activities. No significant changes in renal function were observed in male rats apart from mild enzymuria after a high dose of merbarone (36 mg/kg). The drug did not increase urea nitrogen levels in male or female rats, reflecting the focal nature of this tubular lesion. Merbarone produced small elevations in serum transaminase activities [i.e., glutamic-oxalacetic transaminase (GOT), glutamic-pyruvic transaminase (GPT)] at doses that produced marked alterations in renal function in female rats, suggesting only mild hepatotoxicity. The present study establishes the kidney as a possible dose-limiting target organ for merbarone toxicity.
Cancer Chemother Pharmacol 1989
PMID:Nephrotoxicity of 5-(N-phenylcarboxamido)-2-thiobarbituric acid in the Fischer 344 rat. 259 97

Cis-diamminedichloroplatinum (II) (cisplatin), an inorganic platinum salt used in cancer chemotherapy, is characterized by a renal toxicity recognized both in experimental animals and in patients treated with the compound. The purpose of the present study was to explore by both light and electron microscopy the morphological alterations induced in the rat kidney by cisplatin administration and, in particular, to analyse the tissue repair reaction following nephrotoxic injury. Experimental animals (four rats per group) were treated i.p. with 2, 4 or 8 mg/kg cisplatin administered in four consecutive daily injections. The rats were sacrificed 4 days after the last injection. In addition, the persistence of renal lesions and the duration of the repair reaction were determined in rats given 8 mg/kg cisplatin and killed 4, 7, 14 or 21 days after the last injection. The cell proliferation associated with tissue repair was estimated both quantitatively (rate of DNA synthesis) and qualitatively (histoautoradiography and electron microscopy examination) 1 h after in vivo exposure to [3H] thymidine. Renal tissue alterations and the repair reaction were minimal after the administration of 2 or 4 mg/kg cisplatin. In contrast, 8 mg/kg cisplatin caused a spectrum of morphological abnormalities affecting proximal, distal and collecting tubules, and ranging from sublethal cell alterations to tubular necrosis and cystic dilatation. The latter degenerative change primarily involved the straight portion of proximal tubules and seemed to develop over the weeks following cisplatin administration. Concomitantly with the tissue lesions, a burst of cell proliferation, associated with stimulation of DNA synthesis, was apparent in the renal cortex and outer medulla. Whereas a very high incidence of S-phase cells was encountered in seemingly undifferentiated tubules, they also appeared in differentiated proximal, distal and collecting tubules, but were infrequent in cystic tubules. Proliferation of fibroblasts was also stimulated in the renal interstitium. The proliferative response persisted for the whole duration of the experiment, indicating incomplete tissue repair. The long-lasting tubular injury and the slowness of repair are consistent with the chronic renal dysfunction (polyuria and hypomagnesemia) that cisplatin is known to induce in both man and experimental animals.
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PMID:Tissue injury and proliferative response induced in rat kidney by cis-diamminedichloroplatinum (II). 289 21

A patient who developed hyperosmolar, hyperglycemic, nonketotic coma (HHNC) while receiving home total parenteral nutrient (TPN) therapy is described, and the etiology, clinical features, and treatment of HHNC are reviewed. A 51-year-old black man diagnosed as having Dukes' stage D signet-cell carcinoma of the rectum was discharged on home TPN therapy after a prolonged hospital course and the persistence of a gastrointestinal fistula. Seventeen days after discharge, the patient developed polyuria, became febrile, and lost mental acuity. Upon hospitalization, the patient's physical condition and laboratory values were consistent with the diagnosis of HHNC. The patient was treated with intravenous fluids and small quantities of insulin. The patient's home records indicated that he had lost large volumes of fluid through his fistula, resulting in a net negative fluid balance. The patient's records also indicated that he had had mild glycosuria with a normal urine output at home. This normal urine output despite a body-fluid deficit could be explained by osmotic diuresis related to either glucose or urea. Hypotonic fluid loss resulting from fistula output and osmotic diuresis may have led to this patient's hypertonic state and critical illness. The patient died on hospital day 11 as a result of widely disseminated cancer. HHNC arises most often as a complication of non-insulin-dependent diabetes. It is also a major complication resulting from hypertonicity related to glucose intolerance or other conditions that can occur in patients receiving TPN therapy. The underlying cause of the hyperosmolar state appears to be dehydration.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hyperosmolar, hyperglycemic, nonketotic coma in a patient receiving home total parenteral nutrient therapy. 310 54

Wistar male rats were tested for nephrotoxicity and carcinogenicity after administration of ferric nitrilotriacetate [(NTA) CAS: 139-13-9] (Fe-NTA) [No. of rats (n) = 24] and Al-NTA (n = 24). The control rats were given AlCl3 (n = 10), NTA (n = 10), and saline (n = 10). Sublethal doses of Fe-NTA [5-7 mg Fe/kg (body wt)] and Al-NTA [1.5-2.0 mg Al/kg (body wt)] were chosen and injected ip for 3 months. AlCl3 and NTA were given in equivalent doses and saline was given in equivalent volumes. All the rats given Fe-NTA or Al-NTA had a depressed weight gain, polyuria, and glucosuria from the 1st week. Histologically, acute tubular necrosis and regenerating epithelial cells were observed. Regenerative atypical epithelial cells in the renal cortex were seen at the termination of Fe-NTA or Al-NTA administration. Control rats had no remarkable changes. After 1 year, primary renal cell carcinoma and metastases to liver, lung, and peritoneum were observed only in Fe-NTA-treated rats (14 of 18 surviving rats). On the contrary, there were no tumors in Al-NTA-treated rats (none of 12 surviving rats). The results suggest that nephrotoxicity and renal cell carcinoma are two independent phenomena from Al-NTA treatment and that a long-term sublethal dose of Al-NTA is not related to renal carcinogenicity.
J Natl Cancer Inst 1986 Jan
PMID:Nephrotoxicity and renal cell carcinoma after use of iron- and aluminum-nitrilotriacetate complexes in rats. 345 33

Cis-dichlorodiammine platinum (II), or cisplatin, has emerged as a principal chemotherapeutic agent in the treatment of otherwise resistant solid tumors and is currently among the most widely used agents in the chemotherapy of cancer. The chief limit to its greater efficacy is its nephrotoxicity, which has made it necessary both to lower its dosage and actively hydrate patients to reduce it. The vulnerability of the kidney to cisplatin is almost certainly related to its primary role in the excretion of cisplatin. Cisplatin enters renal cells by a process that depends on normal oxygen utilization and is specifically inhibited by organic bases. Greater localization of platinum to the S3 segment of the proximal tubules suggests that the vulnerability of this segment may depend on its specific uptake of the drug. The majority of intracellular platinum is bound to macromolecules, including protein and DNA, yet a significant portion of cell platinum is biotransformed to a nonmutagenic and possibly nontoxic compound. Polyuria and hypomagnesemia, which are commonly associated with cisplatin nephrotoxicity, may be due to defects in deep nephron or collecting duct fluid and solute transport. Low single nephron glomerular filtration rates (SNGFR) during early cisplatinum-induced acute renal failure is accompanied by reduced renal blood flow and transglomerular hydrostatic pressure without elevated intratubular hydrostatic pressure, suggesting preglomerular vasoconstriction as an important determinant of renal failure.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cisplatin nephrotoxicity. 353 59

A 17-year-old patient with a small paratesticular embryonic sarcoma presented with symptoms of renal failure, polyuria and widespread bone metastases. Investigation revealed hypercalcaemia and uraemia without any evidence of hyperparathyroidism. The hypercalcaemia responded over a period of weeks to administration of mithramycin with initial improvement in the symptoms and metabolic derangements. Control was lost with the necrosis of intra-abdominal tumour deposits and haemorrhagic polypoid deposits in the alimentary tract. The value and hazards of mithramycin are well demonstrated by these rare complications of this type of tumour.
Br J Cancer 1971 Jun
PMID:Mithramycin treatment of hypercalcaemia and renal failure in a patient with paratesticular embryonic sarcoma. 425 8

Ifosfamide and cisplatin are two commonly used cancer chemotherapeutic agents associated with significant acute and chronic renal toxicity. The clinical characteristics of ifosfamide-induced renal injury are proximal tubular wasting of glucose, phosphate, bicarbonate, sodium, potassium, and amino acids; proteinuria; and decreased glomerular filtration rate. Cisplatin administration may result in a dose-dependent reduction of glomerular filtration rate, hypomagnesemia, hypokalemia, and polyuria. The characteristics of renal toxicity associated with each of these agents are discussed with attention to possible mechanisms of injury and long-term clinical outcome.
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PMID:Renal toxicity of cancer chemotherapeutic agents in children: ifosfamide and cisplatin. 778 38

A 24 year old patient with epigastric pain, polyuria, polydipsia and hypercalcemia was admitted to the hospital. Besides the frequent causes of hypercalcemia such as primary hyperparathyroidism and malignancy-related hypercalcemia we had to consider sarcoidosis because of massive splenomegaly. The interstitial lung disease shown on x-ray films of the chest, the epithelioid granulomas in lung tissue and the increased ACE confirmed the diagnosis of sarcoidosis. Hypercalcemia is found in less than 5% of all cases with sarcoidosis. After treatment with steroids, diphosphonates and diuretics all symptoms and the hypercalcemia improved.
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PMID:[Polyuria, polydipsia]. 780 Oct 19


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