Evaluation of the Renal Mechanisms for Urate Homeostasis in Uremic Patients by Probenecid and Pyrazinamide Test

Garyfallos, A.; Magoula, Ifigenia; Tsapas, George

doi:10.1159/000184368

Cited by 29 publications

(22 citation statements)

References 16 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…However, whether these associations are accidental or genetically related could not be elucidated from these cases. As for hyperuricemia, FEUA in all 3 cases was low consistent with the report of Garyfailos et al [11], espe cially in case I, which might suggest the common defect of renal tubular function. Further investigations of this ped igree including HLA typing and chromosome analysis and more information regarding other familial cases are necessary to elucidate the above mentioned problem.…”

Section: Discussionsupporting

confidence: 88%

Unilateral Renal Agenesis Associated with Various Metabolic Disorders in Three Siblings

Uchida

Akiba²,

Sasaki³

et al. 1990

Nephron

View full text Add to dashboard Cite

show abstract

Section: Discussionsupporting

confidence: 88%

Unilateral Renal Agenesis Associated with Various Metabolic Disorders in Three Siblings

Uchida

Akiba²,

Sasaki³

et al. 1990

Nephron

View full text Add to dashboard Cite

show abstract

“…Although the results of these studies should be considered cautiously, but as the same test was used in normo-and hyperuricemic patients, the differences among groups are real. The impairment of secretion of urate could not be a consequence of renal insufficiency, because the decline in the glomerular filtration rate pro duces an adaptative decrease in urate presecretory and postsecretory reabsorption, and a later decrease in urate secretion, but only when creatinine clearance is below 10 ml/min [28], In patients with essential hypertension, hyperuricemia was associated with decreased renal plas ma flow [29] and abnormalities in the handling of urate by the kidney. Similar changes to those found in our patients have been described, and it has been suggested that these could be due to involvement of renal vessels [30], Further more, the association of lower excretion of urate with a tendency to retain water and sodium by the kidney sup port the idea that the hyperuricemia in the renal trans plant patients is probably mediated by hemodynamic changes induced by CyA [31], which could be modified by vasodilators.…”

Section: Discussionmentioning

confidence: 99%

Impairment of Tubular Secretion of Urate in Renal Transplant Patients on Cyclosporine

Marcén

Gallego

Orofino

et al. 1995

Nephron

View full text Add to dashboard Cite

The prevalence of hyperuricemia was investigated in 214 kidney allograft recipients, 81 were on azathioprine and steroids and 133 on cyclosprine (CyA) and low-dose steroids or on triple therapy. All had stable renal function, serum creatinine < 2.5 mg/dl, and a follow-up between 12 and 120 months. At the time of the study, blood and urine samples were obtained to perform tests of renal function. The renal handling of urate was evaluated by a combined pyrazinamide and probenecid test in 35 selected patients (12 normouricemic on azathioprine, 9 normouricemic on CyA and 14 hyperuricemic on CyA). The prevalence of hyperuricemia was higher in the group of patients on CyA (19.7 vs. 66.9%, p < 0.001), as well as the concentration of serum urate (6.1 ± 1.9vs.7.6 ± 1.7, p < 0.001), and serum creatinine (1.2 ± 0.3 vs. 1.4 ± 0.4, p < 0.001). In patients on CyA, multivariate analysis showed that the most important predictive variables of hyperuricemia were: serum creatinine, FE_urate, diuretic use and CyA blood levels (r = 0.73, p < 0.0001). Thirteen patients on CyA (9.9%) had at least one episode of gouty arthritis. Those patients were older than the hyperuricemic patients without gout (45.7 ± 6.7 vs. 37.1 ± 13.5 years, p < 0.01), had worse renal function (serum creatinine 1.9 ± 0.4 vs. 1.5 ± 0.4 mg/dl, p < 0.01), and higher prevalence of hypertension (100 vs. 63.1%, p < 0.05). The combined pyrazinamide-probenecid test showed a lower FE_urate during the maximal probenecid-induced uricosuria (p < 0.05) and a lower urate secretion (p < 0.05) in hyperuricemic patients on CyA than in normouricemic on azathioprine or normouricemic on CyA. There were no differences either in the presecretory reabsorption or in the postsecretory reabsorption. According to the previous results, 20 hyperuricemic patients (11 with gouty arthritis) were treated with benziodarone (50-100 mg/day). At 1 month, there was a decrease in the serum urate (10.1 ± 1.8 vs. 5.1 ± 1.4 mg/dl, p < 0.01), and a parallel increase in FE_urate (7.1 ± 2.4 vs. 25.4 ± 7.4%, p < 0.001), that persisted after 1 year of follow-up. The drug was well tolerated, and we did not observe side effects. The serum creatinine, CyA dose and CyA blood levels remained unchanged. In conclusion, hyperuricemia is a frequent complication in transplant patients on treatment with CyA. Our data suggest that the disorder could be due to an impairment of the tubular secretion of urate. Benziodarone is an alternative to allopurinol for the treatment of this complication, which does not have important side effects.

show abstract

“…[14] The response of urate excretion to drugs that alter renal tubular of urate has been used to analyze the tubular mechanisms of urate transport in man by several authors. [3,4,12,[14][15][16][17][18][19][20][21][22][23] However, secretion and reabsorption may occur in the same tubular segments, and may have active and passive components. Reabsorption of filtered and secreted urate may occur at the same or separate sites and by the same or distinct mechanisms.…”

Section: Discussionmentioning

confidence: 99%

“…The response of urate excretion to PB and PZA has been widely used to analyze the tubular mechanisms of urate transport in normal subjects as well as in patients with renal failure or abnormal urate clearance. [12,13] …”

Section: Introductionmentioning

confidence: 99%

Urate Homeostasis in Polycystic Kidney Disease: Comparison With Chronic Glomerulonephritic Kidney

Mavromatidis¹,

Magoula

Tsapas

2002

Renal Failure

View full text Add to dashboard Cite

Autosomal dominant polycystic kidney disease (ADPKD) might affect urate homeostasis and clearance. Renal tubular urate transport was studied by means of probenecid (PB) and pyrazinamide (PZA) tests in individuals with ADPKD and normal renal function as well as various degrees of renal failure (49 patients). Comparisons were made between polycystic and chronic glomerulonephritic kidney (CGNK), as well as with controls (men with normal renal function). Patients with ADPKD and normal renal function showed plasma urate levels within normal range and normal renal urate handling. In contrast higher plasma urate levels comparing to controls were found in patients with CGNK and normal renal function. During the evolution of renal failure ADPKD patients showed lower urate plasma levels and higher renal clearance as well as, fractional urate excretion, comparing to CGNK patients with the same degree of renal failure. In conclusion patients with ADPKD and normal renal function have normal urate handling and plasma urate levels within normal range. With increasing severity of disease and during evolution of renal failure CGNK patients showed higher urate plasma levels and lower clearances comparing to ADPKD patients. When renal disease becomes more advanced there was no difference in renal urate handling between ADPKD and CGNK patients.

show abstract

Evaluation of the Renal Mechanisms for Urate Homeostasis in Uremic Patients by Probenecid and Pyrazinamide Test

Cited by 29 publications

References 16 publications

Unilateral Renal Agenesis Associated with Various Metabolic Disorders in Three Siblings

Unilateral Renal Agenesis Associated with Various Metabolic Disorders in Three Siblings

Impairment of Tubular Secretion of Urate in Renal Transplant Patients on Cyclosporine

Urate Homeostasis in Polycystic Kidney Disease: Comparison With Chronic Glomerulonephritic Kidney

Contact Info

Product

Resources

About