Renal Handling of Creatinine in Nephrotic and Non-Nephrotic Patients

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
Keyword(s):  
Renal Function ◽  
Normal Subjects ◽  
Tubular Secretion ◽  
Inulin Clearance ◽  
Clearance Ratio ◽  
Renal Handling ◽  
Secretory Rate ◽  
Ureteral Catheterization ◽  
Iothalamate Clearance

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.

scholarly journals Evidence for net renal tubule oxalate secretion in patients with calcium kidney stones

2011 ◽  
Vol 300 (2) ◽  
pp. F311-F318 ◽  
Author(s):  
Kristin J. Bergsland ◽  
Anna L. Zisman ◽  
John R. Asplin ◽  
Elaine M. Worcester ◽  
Fredric L. Coe
Keyword(s):  
Fractional Excretion ◽  
Normal Subjects ◽  
Tubular Secretion ◽  
Idiopathic Hypercalciuria ◽  
Renal Handling ◽  
Stone Formers ◽  
Oxalate Secretion ◽  
Calcium Phosphorus ◽  
Urine Oxalate ◽  
Urinary Oxalate Excretion

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.

Effect of DIDS on renal tubular transport

1980 ◽  
Vol 238 (2) ◽  
pp. F99-F106
Author(s):  
F. J. Koschier ◽  
M. F. Stokols ◽  
J. M. Goldinger ◽  
M. Acara ◽  
S. K. Hong
Keyword(s):  
Transport System ◽  
Organic Anion ◽  
Tubular Secretion ◽  
Inulin Clearance ◽  
Clearance Ratio ◽  
Renal Cortical Slice ◽  
Anion Transport System ◽  
Renal Tubular ◽  
Renal Slice Transport ◽  
Perfused Kidney

Two stilbene derivates that had been used to covalently label the Cl- carrier in the erythrocyte were investigated for reactivity with the renal organic anion system. These compounds, 4,4'-diisothiocyanostilbene-2,2'-disulfonate (DIDS) and (4,4'-diisothiocyano)-dihydrostilbene-2,2'-disulfonate (H2DIDS), were found to be potent inhibitors (Ki congruent to 35 microM) of p-aminohippurate (PAH) transport in the renal cortical slice without affecting tetraethylammonium (TEA) transport or tissue viability. During renal clearance studies performed in the perfused kidney, DIDS decreased the PAH/inulin clearance ratio to congruent to 1. When the possible renal transport of [3H]H2DIDS was investigated, the renal slice transport or binding of [3H]H2DIDS reached a slice-to-medium ratio of congruent to 6, and this accumulation was decreased by probenecid. In perfused kidney experiments, the [3H]H2DIDS/inulin clearance ratio was congruent to 0.8. Since probenecid reduced this clearance ratio to congruent to 0.5, there was the possibility that H2DIDS underwent tubular secretion. In conclusion, DIDS and H2DIDS interacted with the renal organic anion transport system, which indicated that these compounds were possible probes for this transport system.

Cimetidine administration and tubular creatinine secretion in patients with compensated cirrhosis

2001 ◽  
Vol 102 (1) ◽  
pp. 91-98 ◽  
Author(s):  
Giovanni SANSOÈ ◽  
Alberto FERRARI ◽  
Carmen Nives CASTELLANA ◽  
Lorenzo BONARDI ◽  
Erica VILLA ◽  
...  
Keyword(s):  
Oral Administration ◽  
Fractional Excretion ◽  
Tubular Secretion ◽  
Inulin Clearance ◽  
Sodium Reabsorption ◽  
Lithium Clearance ◽  
Clearance Ratio ◽  
Compensated Cirrhosis ◽  
Tubular Sodium Reabsorption ◽  
Sodium Load

Cimetidine inhibits the tubular secretion of creatinine, without altering the glomerular filtration rate (GFR). During cimetidine administration the creatinine/inulin clearance ratio approaches unity in patients with renal failure. We determined the clearance of lithium (an index of fluid delivery to the distal nephron), inulin (a measure of the actual GFR) and creatinine during cimetidine administration to investigate the occurrence of tubular creatinine secretion in patients with compensated cirrhosis. A total of 12 patients with Child-Pugh A cirrhosis were studied initially. The subjects consumed a stable diet containing 100mmol of sodium. On successive days, 9h creatinine clearances were measured, first without and then with the oral administration of cimetidine (400mg as a priming dose, followed by 200mg every 3h). During the first study day, 4h renal lithium clearance was also calculated. A further group of five patients with fully compensated cirrhosis underwent the measurement (on successive days) of plasma inulin clearance, first without and then with the oral administration of cimetidine (same schedule of drug administration). Cimetidine administration unmasked a marked overestimation of GFR when calculated as creatinine clearance (baseline, 138±20ml/min; +cimetidine, 89±13ml/min; P < 0.01). Consequently, during cimetidine administration the calculated lithium fractional excretion (a measure of the fraction of filtered sodium load that is delivered to the loop of Henle) rose from 21.4±13.2% to 32.3±18.9% (P < 0.05), and the ratio between absolute distal tubular sodium reabsorption and filtered sodium load rose from 20.6±13.1% to 31.6±19.3% (P < 0.01). Cimetidine caused no significant decrease in the actual GFR (i.e. inulin clearance) when administered to the second group of patients with compensated cirrhosis. Our data demonstrate significant tubular secretion of creatinine in patients with compensated cirrhosis and, consequently, a marked overestimation of GFR and filtered sodium load and an underestimation of the fractional distal tubular sodium reabsorption when these parameters are calculated by means of the traditional creatinine and lithium clearance computation. The true GFR (measured as inulin clearance) is unaffected by cimetidine administration.

Renal Function in the Spectacled Hare-Wallaby, Lagorchestes conspicillatus: Effects of Dehydration and Protein Deficiency

1983 ◽  
Vol 31 (2) ◽  
pp. 101 ◽  
Author(s):  
HR Bakker ◽  
SD Bradshaw
Keyword(s):  
Renal Function ◽  
Glomerular Filtration ◽  
Protein Intake ◽  
Protein Diet ◽  
Inulin Clearance ◽  
Field Observations ◽  
Clearance Ratio ◽  
Low Protein ◽  
Urine Production ◽  
Protein Diets

Renal function was studied in a marsupial, the spectacled hare-wallaby Lagorchestes conspicillatus, and the effects of acute dehydration and exposure to a low-protein diet assessed. The rate of glomerular filtration (GFR), measured as the inulin clearance, fell significantly with both treatments but tubular function was unaffected. This reduction in GFR accounted entirely for the antidiuresis observed with both dehydration and exposure to low-protein intake and accords with field observations of the hare- wallaby, where urine volumes are characteristically low and have low osmolalities. When data from animals on both high and low-protein diets were considered together, the clearance ratio for urea (C*urea/C*in) was found to be positively correlated with the rate of urine production, and it is evident that mechanisms which invoke antidiuresis in this species will automatically enhance the reabsorption of urea.

Plasma Oxalate Concentration and Renal Excretion of Oxalate in Man

1974 ◽  
Vol 46 (1) ◽  
pp. 61-73 ◽  
Author(s):  
A. Hodgkinson ◽  
R. Wilkinson
Keyword(s):  
Normal Subjects ◽  
Volume Of Distribution ◽  
Mean Value ◽  
Tubular Secretion ◽  
Clearance Ratio ◽  
Oxalate Concentration ◽  
Isotopic Method ◽  
Isotopic Methods ◽  
Renal Tubular ◽  
Normal Men

1. The concentration of oxalate in plasma was determined by an isotopic method involving the simultaneous measurement of [14C]oxalate activities in plasma and urine and the concentration of stable oxalate in the urine. 2. Plasma oxalate concentrations ranged from 1.3 to 1.6 μmol/l (11.8–14.3 μg/100 ml) in three normal men; in fifteen male patients with renal calcium oxalate stones the mean value was 1.73 μmol/l (15.6 μg/100 ml), SD = 0.55 μmol/l (4.98 μg/100 ml). 3. The renal clearance of [14C]oxalate ranged from 162 to 358 ml/min (mean = 249 ml/min) in the normal subjects and from 95 to 315 ml/min (mean = 201 ml/min) in the patients. A direct and statistically significant relationship was observed between the oxalate and creatinine clearances. 4. The oxalate/creatinine clearance ratio ranged from 1.42 to 2.60 (mean = 1.95) in the normal subjects and from 1.04 to 2.33 (mean = 1.76) in the patients, implying a net renal tubular secretion of oxalate. However, oxalate excretion was unaffected by probenecid, a drug known to inhibit the active tubular transport of organic anions. 5. Possible errors in the determination of plasma oxalate concentration and oxalate clearance by chemical and isotopic methods are discussed. 6. Intravenous administration of [14C]oxalate to eight subjects allowed estimations of the miscible oxalate pool [mean = 53.3 μmol (4.80 mg); SD = 18.7 μmol (1.68 mg)], the volume of distribution of [14C]oxalate (mean = 45.2% of body weight; SD = 5.65) and the biological half-life of [14C]oxalate (mean = 91.10 min; SD = 13.89).

Postural Changes in Essential Hypertension under Treatment and their Effect on the Renogram

1971 ◽  
Vol 10 (01) ◽  
pp. 39-46
Author(s):  
C. Alexandrou ◽  
E. Papadakis ◽  
E. Gyftaki ◽  
J. Darsinos
Keyword(s):  
Renal Function ◽  
Essential Hypertension ◽  
Early Diagnosis ◽  
Postural Hypotension ◽  
Antihypertensive Treatment ◽  
Normal Subjects ◽  
Upright Position ◽  
Postural Changes ◽  
Significant Impairment

SummaryRadioisotope renograms were obtained in the upright and prone position in 9 normal subjects, in 5 patients with untreated essential hypertension and in 21 hypertensives under treatment, showing moderate postural hypotension.No significant renographic change were seen in the two positions in normal subjects and untreated hypertensives. Treated hypertensives with postural hypotension showed significant impairment of renal function in the upright position in 15 cases and no change in 6. Renal creatinine clearance was lower in the group that showed renographic changes. Renography in the upright position is suggested as a convenient test for early diagnosis and follow-up of the adverse effects of antihypertensive treatment.

Urinary Beta-Thromboglobulin Correlates with Impairment of Renal Function in Patients with Diabetic Nephropathy

1986 ◽  
Vol 56 (02) ◽  
pp. 229-231 ◽  
Author(s):  
A H Hopper ◽  
H Tindall ◽  
J A Davies
Keyword(s):  
Renal Function ◽  
Diabetic Nephropathy ◽  
Microvascular Disease ◽  
Normal Subjects ◽  
Specific Protein ◽  
Creatinine Concentration ◽  
Β2 Microglobulin ◽  
Plasma Creatinine Concentration ◽  
Insulin Dependent ◽  
Indium 111

SummaryTBeta-thromboglobulin (βTG) is a platelet-specific protein and since its concentration in plasma rises when platelets are activated, it has been used as an indicator of platelet involvement in vascular disease. Since platelets might be involved in the pathogenesis of diabetic microvascular disease we measured urinary βTG in 20 insulin-dependent diabetics with nephropathy and compared the results with those from 20 normal subjects. Measurement of βTG in urine was undertaken to avoid errors induced by blood sampling and to gain information over a prolonged period using a single assay. Measurements were made of βTG, β2-microglobulin and total protein in urine collected for 24 h and creatinine and β2 microglobulin in plasma. Survival of indium-111-labelled platelets was measured in nine patients. Urinary PTG was significantly (p <0.02) increased in the 20 patients compared with 20 normal volunteers (median value 1.3 vs 0.8 μg/24 h). There was a strong correlation between urinary βTG excretion and plasma creatinine concentration (r = 0.8, p <0.0001) and plasma β2-microglobulin concentration (r = 0.9, p <0.0001). Urinary βTG concentration did not correlate with platelet survival. The results indicate that although urinary βTG is significantly increased in patients with diabetic nephropathy its concentration in urine correlates with indicators of glomerular filtration rather than with a test of platelet activation.

Bradykinin and renal function in normal man: effects of adrenergic blockade

1965 ◽  
Vol 209 (4) ◽  
pp. 844-848 ◽  
Author(s):  
John R. Gill ◽  
Kenneth L. Melmon ◽  
Louis Gillespie ◽  
Frederic C. Bartter
Keyword(s):  
Blood Pressure ◽  
Renal Function ◽  
Normal Subjects ◽  
Adrenergic Blockade ◽  
Disease States ◽  
Lower Blood ◽  
Normal Man ◽  
Endogenous Release ◽  
Infusion Of Norepinephrine ◽  
As Effects

Renal function was studied in five normal subjects during the infusion of bradykinin at 0.1 and 0.4 µg/kg per min, and in four additional normal subjects during the infusion of norepinephrine at dosages beginning with 1–3 µg/ min. Bradykinin at both dosages decreased glomerular filtration rate (GFR) and tended to increase renal blood flow (ERPF). It increased sodium excretion (UNaV) at the lower dosage, but did not increase it further at the higher dosage. At all dosages, norepinephrine decreased ERPF and UNaV. The effects of bradykinin cannot be explained solely as effects of norepinephrine released by the bradykinin. During adrenergic blockade produced by guanethidine, bradykinin, 0.1 µg/kg per min, slightly decreased GFR and UNaV; at 0.4 µg/kg per min, it further decreased GFR and UNaV and tended to decrease ERPF as well. It did not lower blood pressure. The data suggest that in normal man, bradykinin increases UNaV only at low dosages. During adrenergic blockade, endogenous release of angiotensin could have prevented bradykinin from lowering blood pressure and could have caused the decreases in GFR, ERPF, and UNaV. A possible role is suggested for bradykinin in the physiologic control of renal function, and as a causative agent in producing the changes in renal function found in certain disease states characterized by excessive production of kinins.

Effects of growth hormone and IGF-I on renal function in rats with normal and reduced renal mass

1990 ◽  
Vol 259 (5) ◽  
pp. F747-F751 ◽  
Author(s):  
S. B. Miller ◽  
V. A. Hansen ◽  
M. R. Hammerman
Keyword(s):  
Growth Hormone ◽  
Renal Function ◽  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Renal Mass ◽  
Filtration Rate ◽  
Inulin Clearance ◽  
Mass Reduction ◽  
Contralateral Kidney ◽  
Igf I

To characterize actions of growth hormone (GH) and insulin-like growth factor ( (IGF-I) on renal function in rats with normal and reduced renal mass, we administered recombinant bovine growth hormone (bGH) or human IGF-I (hIGF-I) to normal rats or to rats that had undergone unilateral nephrectomy and two-thirds infarction of the contralateral kidney, and measured inulin and p-aminohippurate clearances over 10-17 days. Administration of either bGH (100-200 micrograms/day) or hIGF-I (200 micrograms/day) to rats with normal renal mass increased inulin and p-aminohippurate clearances compared with those measured in animals that received vehicle. Filtration fractions were not affected by either bGH or hIGF-I. Inulin clearance was decreased to approximately 17% of normal 1 day after reduction of renal mass in rats. Over the next 3 days insulin clearance increased significantly in rats with reduced renal mass that were administered vehicle. No further enhancement occurred during the next 7 days. Neither bGH nor hIGF-I affected inulin clearance in rats with reduced renal mass. We conclude that both GH and IGF-I enhance glomerular filtration rate when administered to rats with normal renal mass, but not when administered in the same quantities to rats in which renal functional mass is reduced. Glomerular filtration rate increases within 4 days of renal mass reduction independent of exogenous GH or IGF-I.

Elimination of transient secretion of phosphate by alkalinization of plasma in dogs

1961 ◽  
Vol 201 (3) ◽  
pp. 499-504 ◽  
Author(s):  
Gaspar Carrasquer ◽  
William A. Brodsky
Keyword(s):  
Renal Function ◽  
Steady State ◽  
Renal Artery ◽  
Sodium Phosphate ◽  
Tubular Secretion ◽  
Serum Phosphate ◽  
Alkaline Urine ◽  
Urine Acidification

Sodium phosphate and creatinine (500 µmoles each) were injected instantaneously into the renal artery of dogs anesthetized with Nembutal. Urine flows of 6–12 ml/min and serum phosphate levels of 3–6 mm/liter were maintained for 1 hr preceding instantaneous injection. Dogs were divided into two major groups, based on steady state conditions imposed: a) systemic acidosis induced by infusion of NaH2PO4 and b) systemic alkalosis induced by infusion of Na2HPO4 + NaHCO3. Then, either NaH2PO4 or Na2HPO4 was injected close-arterially, and the transient excretory response (covering 3–5 min) was studied. The parameter for measuring renal function was the incremental excretion of phosphate per unit injected per one circulation through the kidney. This was compared to the simultaneous and identical parameter for creatinine, considered as a glomerular substance. During systemic acidosis, net transient secretion of phosphate was observed in 73% of the periods after H2PO4– injection, and in 19% of the periods after HPO4– injection into renal artery. During systemic alkalosis with formation of alkaline urine, net secretion was observed in 15% of the periods after HPO4– injection, and in none of the periods after H2PO4– injection into the renal artery. When paradoxical aciduria occurred during systemic alkalosis, net transient secretion was observed in 30% of the periods after HPO4– injection. Data show that the transtubular movement of H2PO4– ion is different from that of HPO4– ion. The possibility of tubular secretion of H2PO4– ion, as a mechanism of urine acidification, is discussed.

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