The Relationship between Insulin, Glucose and Serum Uric Acid and Their Contribution to the Progression of Renal Damage in Patients with Primary Glomerulonephritis

Manitius, Jacek; Biedunkiewicz, Bogdan; Kustosz, J; Rutkowski, Bolesław

doi:10.1177/030006059602400601

Cited by 5 publications

(3 citation statements)

References 6 publications

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“…6) and in multiple regression analysis (table 2). Manitius et al [13]suggest that purine metabolism may modulate the progression of renal disease in proteinuric patients.…”

Section: Discussionmentioning

confidence: 99%

Serum Uric Acid and Renal Prognosis in Patients with IgA Nephropathy

Ohno

Hosoya

Gomi

et al. 2001

Nephron

158

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Background/Aims: This study was designed to elucidate the clinical significance of serum uric acid (SUA) and the relationship between hyperuricemia and renal prognosis in IgA nepropathy. Methods: The correlation between SUA and other clinical parameters were examined in 748 IgA nephropathy patients (432 males and 316 females). Among these patients, 226 (144 males and 82 females) who were followed for more than 5 years were examined for the relationship between hyperuricemia and renal prognosis. Results: In IgA nephropathy, SUA correlated negatively with creatinine clearance (Ccr), and positively with urinary protein and tubulointerstitial damage. SUA was higher in patients with hypertension or diffuse proliferative glomerulonephritis. Hyperuricemia was a risk factor for renal prognosis, both in terms of serum creatinine (p = 0.0025) and Ccr (p = 0.0057). In 56 patients with normal Ccr at renal biopsy, the change of Ccr after more than 8 years was –22.3 ± 20.8% in 13 patients with hyperuricemia, compared with +2.6 ± 39.4% in 43 patients without hyperuricemia (p = 0.0238). Hyperuricemia was related independently to deterioration of Ccr (p = 0.0461). Conclusion: Hyperuricemia in IgA nephropathy is derived from both glomerular and tubulointerstitial damage, and correlated with hypertension. Hyperuricemia is a risk factor for renal prognosis in IgA nephropathy.

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“…6) and in multiple regression analysis (table 2). Manitius et al [13]suggest that purine metabolism may modulate the progression of renal disease in proteinuric patients.…”

Section: Discussionmentioning

confidence: 99%

Serum Uric Acid and Renal Prognosis in Patients with IgA Nephropathy

Ohno

Hosoya

Gomi

et al. 2001

Nephron

158

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“…In experimental studies it was shown that hyperuricemia-induced tubulointerstitial damage is strongly associated with hypertension and salt sensitivity [4, 5]. Our previous study [6] showed that uric acid may be involved in the progression of renal disease in proteinuric patients. Because intrarenal vessel dysfunction plays crucial role in the damage to the interstitium, it seems reasonable to evaluate the association between uric acid and renal vessel function in patients with IgA nephropathy.…”

Section: Introductionmentioning

confidence: 99%

Uric Acid Excretion and Dopamine-Induced Glomerular Filtration Response in Patients with IgA Glomerulonephritis

Sulikowska

Manitius²,

Odrowąż-Sypniewska³

et al. 2007

Am J Nephrol

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Background/Aim: It is unknown to what extent uric acid (UA) may affect vessel function and participate in tubulointerstitial damage. We examined the relationship between intrarenal vessel function and serum UA and its excretion in association with urinary N-acetyl-β-D-glucosaminidase (NAG). Methods: In 50 IgA patients (mean age 34.7 ± 9.3 years) and 15 controls (mean age 33.5 ± 6.9 years) with a creatinine clearance of 99.4 ± 21.6 and 118.1 ± 17.2 ml/min, respectively, the renal vascular function was estimated based on the dopamine-induced glomerular filtration response (DIR; see text). The DIR was measured using two 120-min creatinine clearance values (before and after intravenous administration of 2 g/kg/min dopamine). Serum UA, triglycerides and cholesterol and urinary NAG (24 h) and protein and UA excretion were measured. Results: Patients with IgA nephropathy versus controls: DIR 8.80 ± 6.6 vs. 12.83% (p < 0.01), NAG 7.25 ± 3.30 vs. 4.69 ± 1.12 U/g creatinine (p < 0.01), and fractional UA excretion 7.80 ± 2.20 versus 6.29 ± 1.80% (p < 0.01). A negative correlation between DIR and NAG was found; regression analysis showed a more prominent relationship in the patients (NAG = 9.99 – 0.29x DIR) than in the controls (NAG = 5.50 – 0.06x DIR). UA and urate excretion and NAG in the patients correlated with DIR (r = –0.39, p < 0.02; r = –0.29, p < 0.04, and r = 0.59, p < 0.001, respectively). Multivariate analysis showed an association of DIR (R² = 0.39) with NAG but not with proteinuria and UA and UA excretion; the NAG excretion (R² = 0.56) correlated significantly with UA and DIR. Conclusion: It is suggested that UA plays a role, associated with tubular dysfunction, in the regulation of intrarenal vessel function.

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“…Blood was collected at 0, 30, 60 and 120 min for uric acid determination. Plasma uric acid area Studies were carried out in 25 untreated pateints with mild primary (essential) hypertension according to the WHO classifica-(PUAA) under the curve was calculated according to a previously used method [17]. tion.…”

Section: Methodsmentioning

confidence: 99%

Hypertensive Nephropathy – An Increasing Clinical Problem

Rutkowski

Tylicki²,

Manitius³

et al. 1999

Mineral Electrolyte Metab

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Arterial hypertension-related renal damage is an increasingly common problem recently, because approximately 25% of patients currently treated with dialysis were hypertensive before renal replacement therapy was started. Hypertension is also known as a metabolic disease, while carbohydrate, purine and lipid disturbances are the features of this syndrome. On the other hand, the progression of renal disease depends on the extent of tubulointerstitial injury. For this reason, we undertook a study to evaluate the relationship between excretion of the markers of tubular damage (NAG) and some parameters of carbohydrate, purine and lipid metabolism in untreated essential hypertension. Both healthy volunteers (n = 15) aged 32.6±7.8 and essential hypertensives (n = 25) aged 37.24±11.39 underwent the same tests. These tests were performed at 2-day intervals: intravenous glucose tolerance test with 0.5 g/kg b.w. as 40% glucose solution and oral fructose load test with 1.0 g/kg b.w. Area under glucose curve (GA) and serum uric acid post-fructose (PUAA) were calculated. Fasting: insulin, total cholesterol and LDL, triglycerides, free fatty acids (FFA) and urine excretion of NAG, albumin were determined. Glomerular filtration rate was estimated as creatinine clearance. Hypertensives showed statistically higher BMI (p<0.007), NAG (p<0.02), total cholesterol (p<0.01), LDL (p<0.007), FFA (p<0.007), insulin (p<0.01), PGA (p<0.01) and PUAA (p<0.03). NAG excretion correlated positively with WHR (r = 0.40), MAP (r = 0.47) and PUAA (r = 0.47) in hypertensives only. We presume that tubular injury at an early stage of renal damage in patients with essential hypertension could be a part of metabolic syndrome X.

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The Relationship between Insulin, Glucose and Serum Uric Acid and Their Contribution to the Progression of Renal Damage in Patients with Primary Glomerulonephritis

Cited by 5 publications

References 6 publications

Serum Uric Acid and Renal Prognosis in Patients with IgA Nephropathy

Serum Uric Acid and Renal Prognosis in Patients with IgA Nephropathy

Uric Acid Excretion and Dopamine-Induced Glomerular Filtration Response in Patients with IgA Glomerulonephritis

Hypertensive Nephropathy – An Increasing Clinical Problem

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