Renal Handling of Hypoxanthine and Xanthine in Normal Subjects and in Cases of Idiopathic Renal Hypouricemia

Author(s):  
Kiyoko Kaneko ◽  
Shin Fujimori ◽  
Takaaki Kanbayashi ◽  
Ieo Akaoka
2009 ◽  
Vol 24 (4) ◽  
pp. 869-871 ◽  
Author(s):  
Kazunari Kaneko ◽  
Naho Taniguchi ◽  
Yuko Tanabe ◽  
Takahide Nakano ◽  
Masafumi Hasui ◽  
...  

Nephron ◽  
1992 ◽  
Vol 61 (4) ◽  
pp. 428-431 ◽  
Author(s):  
Masanori Kawachi ◽  
Norio Kono ◽  
Hiroaki Kiyokawa ◽  
Ikuo Mineo ◽  
Hiromu Nakajima ◽  
...  

2005 ◽  
Vol 20 (7) ◽  
pp. 886-890 ◽  
Author(s):  
Hae Il Cheong ◽  
Ju Hyung Kang ◽  
Joo Hoon Lee ◽  
Il Soo Ha ◽  
Suhnggwon Kim ◽  
...  

1970 ◽  
Vol 38 (5) ◽  
pp. 555-562 ◽  
Author(s):  
C. F. Anderson ◽  
D. M. Jaecks ◽  
H. S. Ballon ◽  
J. R. De Palma ◽  
R. E. Cutler

1. The endogenous creatinine/GFR (inulin or free [57Co]cyanocobalamin or [125I]iothalamate) clearance ratios were determined in ninety-nine non-nephrotic patients and subjects and in sixteen nephrotic patients. The clearance ratios of the nephrotic patients were not significantly different from those of the non-nephrotic patients and normal subjects. 2. The clearance ratios increased as the GFR fell from 176 to below 15 ml/min, then decreased toward unity at lower GFR values. 3. In an attempt to explain this biphasic relationship, two further studies were performed. Endogenous creatinine/inulin and [14C]creatinine/inulin clearance ratios were simultaneously determined in seventeen additional patients. The [14C]creatinine/inulin clearance ratio was the larger of the two in all patients with a GFR greater than 15 ml/min. In another group of eight patients with unequal-sized kidneys, who were studied during bilateral ureteral catheterization, the endogenous creatinine/inulin clearance ratios were determined and found not to differ significantly. 4. The three studies suggest that there is significant tubular secretion of creatinine at all levels of renal function. The increasing clearance ratio of endogenous creatinine/GFR as the GFR decreases is not due to increased tubular secretion of creatinine nor a result of a difference in creatinine handling by diseased kidneys, but rather a reflection of the decreasing fraction of non-creatinine chromogen to the total creatinine chromogen. The smaller clearance ratio at a very low GFR would be expected if the maximal tubular secretory rate of creatinine was exceeded.


2011 ◽  
Vol 300 (2) ◽  
pp. F311-F318 ◽  
Author(s):  
Kristin J. Bergsland ◽  
Anna L. Zisman ◽  
John R. Asplin ◽  
Elaine M. Worcester ◽  
Fredric L. Coe

Little is known about the renal handling of oxalate in patients with idiopathic hypercalciuria (IH). To explore the role of tubular oxalate handling in IH and to evaluate whether differences exist between IH and normal controls, we studied 19 IH subjects, 8 normal subjects, and 2 bariatric stone formers (BSF) during a 1-day General Clinical Research Center protocol utilizing a low-oxalate diet. Urine and blood samples were collected at 30- to 60-min intervals while subjects were fasting and after they ate three meals providing known amounts of calcium, phosphorus, sodium, protein, oxalate, and calories. Plasma oxalate concentrations and oxalate-filtered loads were similar between patients (includes IH and BSF) and controls in both the fasting and fed states. Urinary oxalate excretion was significantly higher in patients vs. controls regardless of feeding state. Fractional excretion of oxalate (FEOx) was >1, suggesting tubular secretion of oxalate, in 6 of 19 IH and both BSF, compared with none of the controls ( P < 0.00001). Adjusted for water extraction along the nephron, urine oxalate rose more rapidly among patients than normal subjects with increases in plasma oxalate. Our findings identify tubular secretion of oxalate as a key mediator of hyperoxaluria in calcium stone formers, potentially as a means of maintaining plasma oxalate in a tight range.


1997 ◽  
Vol 8 (3) ◽  
pp. 445-455 ◽  
Author(s):  
L De Nicola ◽  
V Bellizzi ◽  
B Cianciaruso ◽  
R Minutolo ◽  
G Colucci ◽  
...  

It has been suggested that renal disease is characterized by the presence of resistance to the natriuretic effects of atrial peptide (ANP). In this study, plasma ANP (pANP) and renal function were evaluated during stepwise infusion of low ANP doses (2, 4, 8, and 16 ng/kg per min) in glomerulonephritic patients with (CRF) or without (GN) moderate renal failure, and in normal subjects (NOR), kept at low-sodium diet (LSD; 35 mEq NaCl/day). To assess the physiological ANP levels, pANP was also measured in the three groups after normal-sodium diet (NSD; 235 mEq NaCl/day). ANP did not affect systemic and renal perfusion at any of the doses tested; a significant increment of GFR was observed only in NOR and GN. The 2-, 4-, and 8-ng/kg doses increased pANP to values overlapping the physiological concentrations measured at NSD; this was associated with a dose-dependent increment of urinary excretion of sodium (UNaV) that reached analogous levels in the three groups. ANP accounted for approximately 40% of the UNaV increment evoked by NSD in patients and in normal subjects. The 16-ng/kg dose led to supraphysiological levels that induced a similar marked enhancement of UNaV (from the basal value of 0.12 +/- 0.02 to 0.42 +/- 0.08 mEq/min in CRF, from 0.13 +/- 0.02 to 0.73 +/- 0.08 in GN, and from 0.09 +/- 0.02 to 0.49 +/- 0.11 in NOR). In CRF, the normal natriuretic response to the highest dose was caused by a larger increase of fractional UNaV that was strictly dependent on the greater pANP increment, as demonstrated by similar changes in the fractional excretion of cGMP, and, in part, on the greater aldosterone decrease. In all groups, ANP also induced a dose-dependent urinary loss of phosphate, potassium, and urea, resulting in a significant 15 to 25% decrease in the plasma levels. Thus, in GN and CRF patients, ANP plays a significant role in the renal handling of sodium; moreover, the achievement of low supraphysiological pANP levels leads to a conspicuous natriuresis associated with unique extranatriuretic effects.


Author(s):  
Cuiyu Wang ◽  
Jin Wang ◽  
Song Liu ◽  
Xinhua Liang ◽  
Yifan Song ◽  
...  

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