A micropuncture study of the early phase of acute urate nephropathy.

Conger, John D.; Falk, Sandor; Guggenheim, Stephen; Burke, Thomas J.

doi:10.1172/jci108514

Cited by 57 publications

(30 citation statements)

References 29 publications

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“…The model of acute urate nephropathy is described in detail in a previous report (14). Male Wistar rats and Brattleboro rats, homozygous for hypothalamic diabetes insipidus, and weighing 250-300g, were fasted overnight but permitted free access to water.…”

Section: Methodsmentioning

confidence: 99%

“…An animal model recently developed in our laboratory (14) seemed to lend itself to an investigation of the roles of intrarenal dynamics in the pathogenesis and prevention of acute urate nephropathy. The effects of changes in tubular fluid flow rate, urine pH, and urine osmolality on the magnitude of renal damage from acute hyperuricemia were evaluated in the rat with clearance, micropuncture, and morphologic techniques.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Intrarenal dynamics in the pathogenesis and prevention of acute urate nephropathy.

Conger¹,

Falk²

1977

J. Clin. Invest.

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139

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A B S T R A C T Tubular fluid flow, urine osmolality, and pH were selectively altered to determine the relative protective roles of these factors in a rat model of acute urate nephropathy. Various prehyperuricemic conditions were established in five groups of animals: (a) normopenic Wistar rats given no pretreatment (Group I); (b) Wistar rats given acetazolamide, 20 mg/kg, and isotonic NaHCO3 to produce urine alkalinization (Group II); (c) Wistar rats in which a moderate diuresis, similar to that observed in Group II but without urine alkalinization, was induced with furosemide, 2 mg/kg (Group III); (d) Wistar rats in which a high-flow solute diuresis was induced with furosemide, 15 mg/kg (Group IV); (e) Brattleboro rats, homozygous for pituitary diabetes insipidus, that had a spontaneous high-flow water diuresis (Group V). A comparable level of hyperuricemia (19.4+2.2 mg/100 ml) was achieved in all animals with intravenous urate infusion. Clearance and micropuncture studies were performed before and 1 h after induction of hyperuricemia. Group I rats had mean falls in renal plasma flow and glomerular filtration rate of 83 and 86%, respectively; nephron filtration rate decreased 66%, and tubular and microvascular pressures increased twofold. In Group II there were 45 and 47% declines in renal plasma flow and glomerular filtration rate, respectively, a 66% fall in nephron filtration rate, and a 30% increase in tubular and vascular pressures. Moderate amounts of urate were seen in the kidneys. Group III had changes in renal function identical to Group II suggesting that the moderate prehyperuricemic diuresis in the latter group and not urine alkalinization produced the partial protection observed. Groups IV Portions of this study appeared in abstract form in the

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Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Intrarenal dynamics in the pathogenesis and prevention of acute urate nephropathy.

Conger¹,

Falk²

1977

J. Clin. Invest.

Self Cite

139

View full text Add to dashboard Cite

show abstract

“…In subsequent physiologic experiments in rats, decreased glomerular filtration rate (GFR) in uric acid nephropathy was shown to be secondary to increased efferent arteriolar pressures thought to be secondary to crystal depostion. 33 In two fatal cases of urate nephropathy, uric acid casts were found within the ureters. Similar findings were demonstrated by Wu et al in a genetically-engineered, uric oxidase deficient mouse model.…”

Section: Discussionmentioning

confidence: 99%

Spontaneous tumor lysis syndrome in acute myeloid leukemia: Two cases and a review of the literature

Riccio¹,

Mato²,

Olson³

et al. 2006

Cancer Biology & Therapy

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KEy wORdSspontaneous tumor lysis syndrome, acute spontaneous tumor lysis syndrome, urate nephropathy, tumor lysis syndrome, acute myeloid leukemia, acute renal failure, hyperuricemia ABStRActSpontaneous tumor lysis syndrome (TLS) is a constellation of electrolyte abnormalities and acute renal failure, which occurs in the setting of rapid cell turnover prior to the administration of cytotoxic chemotherapy. While spontaneous TLS is well described in patients with Burkitt's lymphoma, it is thought to occur less commonly in other hematologic malignancies. We present two cases of spontaneous TLS in patients with newly diagnosed acute myeloid leukemia (AML) followed by a review of the literature in this field.

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“…At this low pH, uric acid is 13 times less soluble than at pH 7 (Klinenberg et al, 1965) and the threshold at which uric acid precipitates into crystals may be reached. Crystals obstruct urine flow in the tubules leading to obstructive uropathy (Rieselbach, 1964;Klinenberg et al, 1975;Conger et al, 1976). A uric acid: creatinine greater than 1 is indicative of uric acid nephropathy, whereas a ratio less than 0.6 to 0.75 suggests renal failure of another etiology.…”

Section: Hyperuricemiamentioning

confidence: 99%

Tumour Lysis Syndrome: Implications for Cancer Therapy

Mika¹,

Ahmad²,

Guruvayoorappan³

2012

Asian Pacific Journal of Cancer Prevention

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Asian Pacific J Cancer Prev, 13, 3555-3560 IntroductionTumour lysis syndrome (TLS) is the development of an array of metabolic disturbances that may occur either spontaneously or in response to cancer therapies. It results when a huge number of rapidly dividing cancer cells, particularly leukemia and lymphoma, are killed or lysed by cytotoxic therapy such as chemotherapy and radiation. Normal intracellular components of cells include potassium, phosphorus and nucleic acids. These intracellular ions are present in large amounts in cancer cells as compared to those in normal cells.When malignant cells are killed by therapy they release their contents into the systemic circulation, which accumulate faster in the body than being eliminated from the body and the body's homeostatic mechanisms find it difficult to cope with. The release of these intracellular contents cause metabolic disturbances, which in turn manifest into life threatening complications such as hyperkalemia, hyperphosphotemia, hypocalcemia and hyperuricemia. Tumour lysis also releases cytokines that cause a systemic inflammatory response syndrome and often multiorgan failure (Hijiya et al., 2005;Nakamura et al., 2009;Soares et al., 2009).During the early stages, some patients do not experience any symptoms of TLS but have abnormal laboratory values, which is suggestive of its succession. Laboratory results will show high potassium, uric acid and phosphorus levels and low calcium levels in the blood.

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A micropuncture study of the early phase of acute urate nephropathy.

Cited by 57 publications

References 29 publications

Intrarenal dynamics in the pathogenesis and prevention of acute urate nephropathy.

Intrarenal dynamics in the pathogenesis and prevention of acute urate nephropathy.

Spontaneous tumor lysis syndrome in acute myeloid leukemia: Two cases and a review of the literature

Tumour Lysis Syndrome: Implications for Cancer Therapy

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