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At least 19 recordsLinked to original sources
PubMed1978

A rapid method for the diagnosis of acute uric acid nephropathy.

Acute uric acid nephropathy is a reversible type of renal failure that results from the deposition of uric acid crystals in the collecting tubules. The present study has compared a number of laboratory tests in 5 patients with a clinical diagnosis of this disorder and 27 patients with acute renal failure of other causes. Neither the serum creatinine, BUN, serum urate concentrations, nor the ratio of serum urate:BUN differentiated between these two groups of patients. However, the ratio of uric acid to creatinine concentration on a random urine specimen did differentiate between these two patient populations. All patients with uric acid nephropathy had a ratio greater than 1.0, while all patients with other types of acute renal failure had ratios of less than 1.0.

Acute Kidney Injury↗
PubMed2025

Network pharmacology combined with ultra-high-performance liquid chromatography-quadrupole time-of-flight mass spectrometry method to explore the mechanism of Shizhi Fang in treating uric acid nephropathy mice.

OBJECTIVE: To elucidate the potential mechanisms of Shizhi Fang (SZF, ) in the treatment of uric acid nephropathy (UAN). METHODS: SZF-containing serum was prepared from six male rats and analyzed using ultra-high-performance liquid chromatography-quadrupole time-of-flight mass spectrometry (UPLC-Q-TOF-MS). Network pharmacology was employed was integrated with UPLC-Q-TOF-MS to predict SZF targets for the treatment of UAN, which were subsequently validated through in vivo experiments. Sixty male Bagg Albino Laboratory-Bred Mouse, substrain c mice were randomly allocated into six groups: Normal, Model, Febuxostat, and three SZF dosage groups. Except for the Normal group, all mice were administered potassium oxonate (250 mg/kg) and adenine (50 mg/kg) via gavage to induce UAN. Four hours post-administration, the Febuxostat group received Febuxostat (6 mg/kg), while the SZF groups received low (0.234 g/kg), medium (0.468 g/kg), or high (0.936 g/kg) doses of SZF. The Normal and Model groups were given an equivalent volume of saline. All treatments were conducted over a period of four weeks. Urine and blood samples were collected for biochemical analysis, and kidney tissues were subjected to histopathological examination and Western blot analysis. RESULTS: Nine prototype compounds and 30 metabolites were identified in SZF serum. Network pharmacology analysis revealed 195 drug targets and 1608 disease targets, with 76 common drug-disease targets, including signal transducer and activator of transcription 3 (STAT3), proto-oncogene tyrosine-protein kinase Src (SRC), matrix metalloproteinase-9 (MMP9), Caspase 3, and toll-like receptor 4 (TLR4) as key targets. Gene Ontology analysis identified 325 biological processes, 48 cellular components, and 72 molecular functions, while Kyoto Encyclopedia of Genes and Genomes analysis identified 113 pathways. Molecular docking demonstrated strong binding affinities between active compounds and their targets. In the animal study, SZF treatment alleviated pathological damage and improved serum and urine biochemical markers compared to the Model group (P < 0.05, P < 0.01, P < 0.001). Western blot analysis showed a significant reduction in phosphorylated-STAT3, phosphorylated-SRC, MMP9, TLR4, and Caspase3 expression in renal tissues of SZF-treated mice (P < 0.001). CONCLUSION: SZF may exert therapeutic effects on UAN through multiple targets and pathways.

Animals↗
PubMed1975

Acute uric acid nephropathy in thalassaemia.

Hyperuricaemia may complicate thalassaemia and may, on occasion, result in obstruction of urine flow on the basis of crystal formation. Prophylactic therapy with xanthine oxidase inhibitors may prevent this complication, but once it has developed, accurate diagnosis and aggressive therapy can reduce morbidity. The present case report illustrates one approach to the management of acute uric acid nephropathy.

Adult↗
PubMed1978

Use of the uricase-inhibited rat as an animal model in toxicology.

An accessible, reproducible, and inexpensive animal model for toxicologic evaluation of hyperuricemic conditions has been required for some time. A number of authors have tried to develop such a model by administering high doses of uric acid to various animal species (dog, rabbit, rat) but the potent liver uricase in these species prevented development of sustained hyperuricemia. Johnson et al. [4], Stavric et al. [5], and a number of other investigators [72, 75] successfully used potassium oxonate [63] to block the effect of hepatic uricase and to produce hyperuricemia in rats [4, 5, 68, 69, 72, 74, 76, 80], rabbits [66], mongrel dogs [67], mice [65], and pigs [64]. The oxonate-treated rat can serve as a useful animal model not only in investigation of the uric acid nephropathy, but also in a number of other toxicologic evaluations connected with uric acid. This model has been used to evaluate drugs that affect uric acid excretion, to determine which dietary factors affect serum urates, or to evaluate possible therapeutic agents in certain disorders associated with uric acid. The same model could also be used by behavioral scientists, for whom research on uric acid has become increasingly popular in recent years [33, 137]. The ideal uricase inhibitor for induction of hyperuricemia would be one which is irreversible, noncompetitive, and relatively nontoxic, so that its activity would be independent of high levels of uric acid, and effective inhibition could be attained at low dosage levels. Oxonic acid is not an ideal uricase inhibitor, because it is competitive and is eliminated from the body relatively rapidly. Although relatively nontoxic, oxonic acid and its salts are foreign substances that could interfere with some other metabolic systems. The possibility exists that an ideal, or at least a better inhibitor, could be developed by appropriate substitutions on the molecule of oxonic acid or by introducing different types of compounds such as derivatives of diazohypoxanthines, barbiturates, or similar substances. Until such improvements on the uricase-inhibited rat models are available, potassium oxonate, which is easily obtainable, can be used as an effective inhibitor of uricase in vivo.

Aggression↗
PubMed1978

Hyperuricemia in congenital heart disease.

Gout is rarely noted as a clinical problem in secondary polycythemia-- even if profound polycythemia exists, as in cyanotic congenital heart disease. A retrospective study of 81 patients with congenital heart disease was done to assess the incidence of hyperuricemia. Twenty of 46 patients with cyanotic congenital heart disease had serum levels of uric acid greater than 8 mg/dl. Thirteen of 16 (81%) cyanotic male patients more than 15 years old had serum levels greater than 8 mg/dl. For cyanotic patients, serum levels of uric acid were related directly to the degree of polycythemia (r = .44; P less than .02). Impaired renal function or drug therapy did not seem to account for the hyperuricemia. Because levels of uric acid greater than 10 mg/dl probably are nephropathic, many of these patients may be incurring subclinical uric acid nephropathy.

Adolescent↗
PubMed1978

Acute renal failure in patients with acute leukemia.

Acute renal failure may be a contributory cause of death in patients with acute leukemia. The purpose of this study was to define the causes and course of acute renal failure in group of patients with acute leukemia in order to identify preventive measures and reversible aspects of the renal insufficiency. Among 88 patients with acute leukemia whose courses were followed to the time of death, ten developed acute renal failure. Etiologic factors of the renal failure were uric acid nephropathy, sepsis with complicating hypotension and hypovolemia, and the administration of nephrotoxic antibiotics. In one patient ureteral obstruction from clots was responsible for renal failure, while in another patient disseminated aspergillosis led to renal failure. Other causes of acute renal failure in persons with acute leukemia, but not observed in this patient group, are hypercalcemia and leukemic infiltration of the kidneys.

Acute Disease↗
PubMed1977

Hyperphosphatermia and hypocalcemia accompanying rapid cell lysis in a patient with Burkitt's lymphoma and Burkitt cell leukemia.

Hyperphosphatemia, hypocalcemia and acute oliguric renal failure resulting from uric acid nephropathy developed in a patient with Burkitt's lymphoma and Burkitt cell leukemia after effective chemotherapy. A review of other reported cases in which the patients had similar metabolic abnormalities is presented, and the pathophysiology is discussed. The clinical setting in which these metabolic developments are most likely to occur is defined, and an approach for their prevention and management is presented.

Acute Kidney Injury↗
PubMed1975

Early detection of acute rejection in renal allografts using radioiodinated autologous fibrinogen.

131I-labeled autologous fibrinogen was used to detect acute renal allograft rejection in the early postoperative period. Ratios of radioactive counts over transplanted kidneys to those over the heart increased with deposition of radioactive fibrinogen in kidneys undergoing rejection. The test was positive in all instances of acute rejection twelve to twenty-four hours prior to clinical ro biochemical changes. False-positive test results were noted in instances of perinephric hematoma, seroma, and wound abscess and in one patient with urinary tract infection. The test was negative in cases of renal failure secondary to acute tubular necrosis, uric acid nephropathy (in the absence of acute rejection), and chronic rejection. This test is simple, rapid, and practical. It can be performed at the bedside and is free from complications, particularly serum hepatitis.

Acute Disease↗
PubMed1977

Implications of disorders of purine metabolism for the kidney and the urinary tract.

The spectrum of kidney and urinary tract disorders related to purines comprises acute hyperuricosuric nephropathy, chronic urate nephropathy and urolithiasis. Two factors in the development of acute hyperuricosuric nephropathy are increased uric acid concentration and low pH in the tubular fluid. Chronic urate nephropathy still possess several problems: incidence (although this seems to be decreasing, presumably owing to effective prevention), the source of interstitial urate, the cause of the interstitial deposition of urate, and the role of urate deposits in the pathogenesis of the interstitial nephropathy. The relation of the experimental nephropathy to the pathogenesis of chronic urate nephropathy in the human is not yet clear but a model is proposed according to which interstitial urate derives from two sources: hyperuricaemic plasma and hyperuricosuric tubular fluid. Urolithiasis related to purines leads to uric acid-urate stones, xanthine stones, 2,8-dihydroxyadenine stones, iatrogenic xanthine and oxipurinol stones, and possibly calcium stones. Pathogenetic factors in uric acid lithiasis are hyperuricosuria (whether due to an inborn enzyme abnormality or of unknown aetiology) and low urinary pH; oliguria is a contributory factor. There remain several open questions about uric acid lithiasis: incidence, the shift of its location from lower to upper urinary tract, the interplay of pathogenetic factors, and the role of compounds which inhibit crystallization.

Adenine Phosphoribosyltransferase↗
PubMed1978

[Diagnostic value of renal urate excretion].

After a short survey of the purine metabolism, excretion of uric acid, theories of gout and urate nephropathy methodical references are given for the estimation of excretion of uric acid, a normal region on test persons was established and compared with other authors. The quantities of excretion and concentrations of uric acid from the 24 hours urine found on patients with asymptomatic hyperuricemia and manifest gout are the basis of the discussion of the diagnostic and therapeutic value of these examinations. In patients with gout and asymptomatic hyperuricemia the excretions of uric acid are a little higher than in healthy persons. A treatment with uricosuric remedies might not reduce the factor of risk hyperuricemia, since this does not lead to a prevention of the gout nephrophathy, on the contrary it furthers it.

Adult↗
PubMed1975

Chronic experimental hyperuricemic nephropathy.

Sustained, moderately severe hyperuricemia and severe uricosuria were produced in male Wistar rats by feeding dietary supplements of oxonic acid (0.4 gm. per day) and uric acid (0.6 gm per day). After 1 month, the kidneys showed the previously described histologic features of urate-blockade nephropathy characterized by intratubular deposits, tubular injury, and an exudative response consisting of neutrophilic granulocytes with early tophus formation. After 36 and 52 weeks of hyperuricemia, and with no gross evidence of renal failure, the kidneys showed a predominantly interstitial mononuclear cell infiltrate around regenerated tubules, an increase in interstitial fibrous tissue, infrequent renal tophi, and renal stones. The glomeruli and blood vessels appeared completely normal. There was no evidence of arthritis and no other target organ damage was detected. The chronic renal changes present in this animal model of induced hyperuricemia resemble those seen in human gouty nephropathy. The evolution of the experimental urate nephropathy observed during 1 year suggests that a primary acute inflammatory tubular injury is followed by a diffuse chronic interstitial nephritis and that the glomeruli and blood vessels are not primarily involved in the renal disease. This animal model may provide the opportunity to study factors influencing the renal sequelae of sustained hyperuricemia.

Animals↗
PubMed1978

Acute renal failure. Association with administration of radiographic contrast material.

Fourteen cases of acute renal failure secondary to administration of radiographic contrast media were observed, eight within a 15-month period. No patient had multiple myeloma, and only three were diabetic. Predisposing factors included renal hypoperfusion, preexisting renal insufficiency, hyperuricemia, age of more than 60 years, solitary functioning kidney, and exposure to several contrast studies at closely spaced intervals. Control of blood volume and serum uric acid, appropriate spacing of radiographic studies, and possibly urinary alkalinization and hypouricosuric drugs in high-risk patients are recommended to decrease the incidence and morbidity of contrast-mediated nephropathy.

Acute Kidney Injury↗
PubMed1977

[Acute kidney failure as a complication of fasting therapy].

Acute urate nephropathy during starvation for weight reduction has been observed in 2 patients. Under these conditions ketoacidosis causes impaired renal uric acid excretion and hyperuricemia. Uricosuric agents or sudden intake of normal calorie diet induces massive uricosuria and kidney damage. Uricosuric agents should be avoided and steps taken to promote abundant diuresis, while allopurinol should be prescribed.

Acidosis↗