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Query: UMLS:C0035078 (renal failure)
 31,970 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Polyuria of diabetes insipidus and psychogenic polydipsia can produce massive dilatation of the urinary tract in the absence of any mechanical obstruction. Renal failure in these cases is rare. We report the second case of nephrogenic diabetes insipidus with nonobstructive hydronephrotic renal damage. Temporary suprapubic drainage restored renal function to normal and decreased the upper tract dilatation. Renal function has been preserved for more than 10 years. Surgical intervention beyond temporary vesical drainage is unnecessary.
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PMID:Polyuric urinary tract dilatation with renal damage. 335 42

Familial juvenile nephronophthisis (FJN) is a frequent cause of chronic renal failure in children and adolescents. Typically it presents after 6 years of age through adolescence, but may become apparent in early childhood. The clinical presentation is insidious, and the early symptoms of polyuria and polydipsia are often overlooked in the presence of a relatively normal urinalysis and in the absence of proteinuria, azotemia, and hypertension. Thus most patients are not diagnosed until after the onset of renal failure. These children are excellent candidates for properly selected transplantation.
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PMID:Familial juvenile nephronophthisis. A review and differential diagnosis. 351 Jul 94

Familial juvenile nephronophthisis (FJN) represents an important cause of chronic renal insufficiency in the first two decades of life. Its frequency is reported to vary between 7 and 20% of all cases of terminal renal failure in childhood. Usually the onset is insidious, with polyuria, polydipsia and anaemia being the main clinical features. The diagnosis is based on clinical, laboratory and pathological findings. The purpose of our report is to emphasize the importance of this pathological entity with respect to the clinical symptoms and signs and diagnostic approach on the basis of the case reports of four patients.
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PMID:[Familial juvenile nephronophthisis--a cause of chronic renal failure in childhood]. 352 15

The authors have presented a review of literature and their own data on acute tubulointerstitial nephritis combined with uveitis in a patient aged 47. In foreign literature this combination is defined as a separate syndrome (TIN-uveitis or TINU). The development of nonspecific symptoms (fatigue, weakness, nausea, loss of body mass, pains in the joints, skin rash) was characterized by change in some laboratory indices (raised ESP, anemia, eosinophilia, hyperproteinemia, hypergammaglobulinemia) and nephropathy. The signs of nephropathy were polyuria, a decrease in relative urine density, proteinuria of tubular genesis, renal glucosuria and aminoaciduria. A decrease in glomerular filtration and an increase in the level of blood serum creatinine were noted in most of the cases. In spite of the development of renal failure TINU prognosis is favorable: renal function gets back to normal by itself or after corticosteroid therapy. Uveitis shows a tendency to recurrence. The immune genesis of the TINU syndrome is assumed.
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PMID:[Acute tubulo-interstitial nephritis combined with uveitis (clinical case and review of the literature)]. 353 15

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

Administration of cisplatin (5 mg/kg) to dogs results in polyuric renal failure due initially to a proximal tubular functional impairment. 48-72 h after the cisplatin administration the depressed renal function can be attributed to impairment of proximal as well as distal tubular reabsorptive capacities associated with increased renal vascular resistance. The polyuria seems to be due to the impaired reabsorption rate in the distal nephron segments.
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PMID:Effect of cisplatin on renal haemodynamics and tubular function in the dog kidney. 358 22

To assess a possible role of prostaglandins in the early phase of cisplatin-induced abnormalities in renal concentrating ability, three groups of rats were studied. In a first group we measured prostaglandin production from renal medullary microsomes isolated from rats sacrificed at different time periods after cisplatin, 5 mg/kg alone (PB/CP) or cisplatin plus aspirin, 300 mg/kg p.o., 1 h before cisplatin and daily (ASA/CP). In a second group of rats, balance studies were performed in PB/CP and ASA/CP animals for 4 days after cisplatin to determine the effect of such treatment on the renal excretion of solute and water. In another group of rats inulin clearance was measured in PB/CP and ASA/CP animals 4 days after such treatment. The rats received aspirin or phosphate buffer alone (50 mg/ml sodium phosphate, pH 8) to determine the effect of such treatment on prostaglandin production and renal function. In PB/CP Uosm fell and prostaglandin synthesis increased on days 1-3. Prostaglandin synthesis returned to baseline values by day 4, but Uosm remained low. Inulin clearance was low 4 days after cisplatin. In ASA/CP rats prostaglandin synthesis did not increase and the early polyuria was ameliorated. Aspirin did not prevent the later polyuria. Inulin clearance in the ASA/CP group was markedly reduced to levels below those observed with cisplatin alone. These data demonstrate that elevated rates of prostaglandin synthesis occur early in the course of cisplatin-induced renal failure and suggest that prostaglandins may play a role in the early cisplatin-induced concentrating defect.
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PMID:The role of prostaglandins in early polyuria induced by cisplatin in the rat. 360 Sep 18

Case records from 21 dogs with hypercalcemia and hyperparathyroidism were evaluated. The dogs were greater than or equal to 7 years old, and 6 were Keeshonds. The most common clinical signs were polydipsia/polyuria, listlessness, and muscle weakness. The serum calcium concentrations were 12.1 to 19.6 mg/dl. Serum phosphorus concentrations were low in 5 dogs, within the reference range in 13 dogs, and high in 3 dogs that also had high concentrations of BUN. Twenty dogs had a parathyroid adenoma, and 1 had a parathyroid carcinoma. Nineteen dogs had their parathyroid tumor surgically removed. Within 5 days of tumor removal, 11 of the 19 dogs became hypocalcemic and the remaining 8, normocalcemic. Nine of the 11 hypocalcemic dogs developed clinical signs. Iatrogenic hypercalcemia was induced in 7 of 16 dogs treated orally with calcium carbonate plus vitamin D. Only 1 of 19 dogs that had their parathyroid tumor excised died in hypocalcemic tetany. Two additional dogs died within 2 weeks of surgery, one because of pancreatitis, the other due to renal failure. Eight dogs died 9 to 37 months after surgery of unrelated problems. Eight dogs were alive for at least 7 to 28 months after surgery.
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PMID:Primary hyperparathyroidism in dogs: 21 cases (1976-1986). 365 3

Nephrogenic diabetes insipidus usually presents with polyuria, polydipsia, fever, vomiting, dehydration and failure to thrive. However, in infancy polyuria may be absent because of dehydration and reduced glomerular filtration rate. In 2 cases the main presenting feature was hypotonia, with marked head lag. Family studies confirmed the X-linked mode of inheritance of the disease; in case 1 the disease appeared to have arisen as a new mutation in the mother, and in case 2 the carrier status was traced back to the great-grandmother. Pitfalls in the diagnosis and detection of the carriers are discussed. Treatment with thiazide diuretics and prostaglandin synthesis inhibitors is effective in reducing urine volumes and polydipsia. The early detection of the disease and adequate management may prevent such complications as megacystis, mega-ureter and hydronephrosis, with resulting renal failure. Mental and physical retardation may also be avoided.
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PMID:Nephrogenic diabetes insipidus presenting with infantile hypotonia. A report of 2 cases. 373 62

In male Wistar rats, renal adenosine triphosphate (ATP), inorganic phosphate (Pi) and intracellular pH were measured by 31phosphorus nuclear magnetic resonance (31P NMR) and correlated with renal function before, during, and for one hour after a period of 30 to 40 minutes hemorrhagic hypotension. In animals which suffered no change in these metabolites during hypotension, retransfusion immediately restored normal renal function. When metabolite changes were observed during hypotension, they occurred suddenly with severe ATP depletion, Pi accumulation, and intracellular acidosis occurring almost concurrently. Metabolic changes of this magnitude were always associated with renal dysfunction in the post-hypotensive period, which occurred even when the period of biochemical change was only 10 to 15 minutes. The abnormalities in post-hypotensive renal function resemble the pattern of change seen in human acute tubular necrosis (ATN): depressed glomerular filtration rate (GFR), urine output varying from polyuria to oliguria, decreased urine to plasma inulin ratio, increased urinary sodium concentration, increased fractional excretion of sodium, and increased fractional excretion of potassium. It is postulated that changes in renal cellular energy status during hemorrhagic hypotension distinguish pre-renal failure from early or incipient ATN.
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PMID:Acute renal failure in hemorrhagic hypotension: cellular energetics and renal function. 378 80


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