Sodium and Water Excretion in Nephrotic Patients: Effects of Changes in Renal Haemodynamics

1990 ◽  
Vol 79 (2) ◽  
pp. 123-129 ◽  
Author(s):  
Michael Allon ◽  
Charles B. Pasque ◽  
Mariano Rodriguez

1. Eight nephrotic patients were studied in order to evaluate the effects of acute changes in renal plasma flow and glomerular filtration rate on renal solute and water handling, in the absence of plasma volume expansion. 2. The subjects were studied first after the administration of captopril, a manoeuvre that increased renal plasma flow without a significant change in glomerular filtration rate, and a second time after receiving combined therapy with captopril and ibuprofen, a manoeuvre that decreased glomerular filtration rate without a significant change in renal plasma flow. 3. After captopril therapy, despite the increase in renal plasma flow, there was no significant change in proximal sodium reabsorption (as estimated from fractional lithium reabsorption), urine volume or urine osmolality. 4. The decrease in glomerular filtration rate observed after the administration of captopril plus ibuprofen was associated with decreases in fractional excretion of sodium and urine volume, and an increase in urine osmolality. The changes in these parameters of tubular function were proportionate to the changes in glomerular filtration rate. Fractional proximal sodium reabsorption increased substantially. 5. These observations suggest that, in the absence of plasma volume expansion, an increase in renal plasma flow does not increase sodium or water excretion by the nephrotic kidney. Moreover, during acute decreases in glomerular filtration rate, glomerulotubular balance appears to be disrupted, resulting in disproportionately high rates of proximal tubule sodium reabsorption.

1982 ◽  
Vol 243 (3) ◽  
pp. F300-F305 ◽  
Author(s):  
C. Baylis

Whole kidney and single nephron indices of glomerular ultrafiltration were measured by clearance and micropuncture techniques in anesthetized virgin, 9-day pregnant, and 9-day pseudopregnant Munich-Wistar rats. Whole kidney glomerular filtration rate (GFR) and single nephron glomerular filtration rate (SNGFR) were elevated in pregnant and pseudopregnant rats compared with virgins (0.78 +/- 0.05, 0.75 +/- 0.06 vs. 0.57 +/- 0.03 ml/min, P less than 0.005 and P less than 0.001; 32.1 +/- 2.5, 30.0 +/- 2.8 vs. 22.1 +/- 2.0 nl/min, P less than 0.01 and P less than 0.05, respectively). Total renal plasma flow rate (RPF) and single glomerular plasma flow rate (QA) were also increased in pregnant and pseudopregnant rats compared to virgins (3.05 +/- 0.19, 2.90 +2- 0.24 vs. 2.28 +/- 0.21 ml/min, P less than 0.01 and P less than 0.05; 109.0 +/- 15.8, 100.4 +/- 12.8 vs. 68.0 +/- 6.9 nl/min, both P less thn 0.05). There was little difference in the other determinants of ultrafiltration among the three groups. Plasma volume was measured in separate experiments and was higher in pregnant and pseudopregnant rats compared with virgins (9.4 +/- 0.2, 9.8 +/- 0.4 vs. 8.4 +/- 0.3 ml, P less than 0.01 and P less than 0.05, respectively). The gestational increase in GFR in the rat occurs as the result of increased RPF, which is due to both plasma volume expansion and renal vasodilation. Since the changes in renal hemodynamics seen in pseudopregnancy were almost identical to those occurring in pregnant rats, the early stimulus to increased GFR must be maternal and not fetoplacental in origin.


1976 ◽  
Vol 50 (3) ◽  
pp. 165-169 ◽  
Author(s):  
M. O. Farber ◽  
J. J. Szwed ◽  
A. R. Dowell ◽  
R. A. Strawbridge

1. Effective renal plasma flow, glomerular filtration rate and cardiac output were measured in osmotically loaded dogs before and during comparable acute respiratory and metabolic acidosis. 2. Urine output increased in control dogs and in animals with metabolic acidosis, but declined with respiratory acidosis. Effective renal plasma flow and glomerular filtration rate declined with respiratory and metabolic acidosis. 3. When respiratory acidosis was buffered with sodium bicarbonate, urine volume increased and glomerular filtration rate and effective renal plasma flow were unchanged; with trihydroxymethylaminomethane, urine volume increased but glomerular filtration rate and effective renal plasma flow fell. 4. When metabolic acidosis was buffered with sodium bicarbonate, urine volume increased; with trihydroxymethylaminomethane, urine volume increased but glomerular filtration rate fell. Cardiac output declined only during metabolic acidosis, both buffered and unbuffered. 5. These studies demonstrate that, even with osmotic loading: (1) respiratory acidosis causes a decrease in glomerular filtration rate, effective renal plasma flow and urine volume; (2) metabolic acidosis depresses glomerular filtration rate and effective renal plasma flow but does not change urine volume even though cardiac output falls; (3) sodium bicarbonate is more effective than trihydroxymethylaminomethane in preserving renal function during respiratory and metabolic acidosis.


1971 ◽  
Vol 10 (01) ◽  
pp. 16-24
Author(s):  
J. Fog Pedersen ◽  
M. Fog Pedersen ◽  
Paul Madsen

SummaryAn accurate catheter-free technique for clinical determination simultaneouslyof glomerular filtration rate and effective renal plasma flow by means of radioisotopes has been developed. The renal function is estimated by the amount of radioisotopes necessary to maintain a constant concentration in the patient’s blood. The infusion pumps are steered by a feedback system, the pumps being automatically turned on when the radiation measured over the patient’s head falls below a certain preset level and turned off when this level is again readied. 131I-iodopyracet was used for the estimation of effective renal plasma flow and125I-iothalamate estimation of the glomerular filtration rate. These clearances were compared to the conventional bladder clearances and good correlation was found between these two clearance methods (correlation coefficients 0.97 and.90 respectively). The advantages and disadvantages of this new clearance technique are discussed.


1991 ◽  
Vol 81 (2) ◽  
pp. 271-279 ◽  
Author(s):  
P. G. McNally ◽  
F. Baker ◽  
N. Mistry ◽  
J. Walls ◽  
J. Feehally

1. Nifedipine ameliorates cyclosporin A-induced renal impairment in surgically intact (two-kidney) rats. This study investigates the effect of nifedipine on cyclosporin A nephrotoxicity in spontaneously hypertensive rats after either uninephrectomy or uninephrectomy with contralateral renal denervation. 2. Fourteen days after uninephrectomy pair-fed rats were injected for 14 days with cyclosporin A (25 mg/kg body weight) via the subcutaneous route and with nifedipine (0.1 mg/kg body weight) via the intraperitoneal route. Renal and systemic haemodynamics were measured in conscious unrestrained rats. 3. Whole-blood levels of cyclosporin A did not differ between groups (overall 352 ± 22 ng/ml, means ± sem). After uninephrectomy, cyclosporin A decreased the glomerular filtration rate (olive oil versus cyclosporin A: 0.96 ± 0.04 versus 0.70 ± 0.06 ml min−1 100 g body weight, P < 0.02) and effective renal plasma flow (1.94 ± 0.10 versus 1.38 ± 0.13, P < 0.01), and increased renal vascular resistance {(20.2 ± 1.8) × 104 versus (31.6 ± 3.3) × 104 kPa l−1 s [(20.2 ± 1.8) × 103 versus (31.6 ± 3.3) × 103 dyn s cm−5], P < 0.02} and mean arterial pressure (146.7 ± 6.7 versus 167.3 ± 2.9 mmHg, P < 0.05). Neither renal denervation nor nifedipine prevented the reduction in glomerular filtration rate or effective renal plasma flow induced by cyclosporin A. 4. This study infers that the sympathetic nervous system does not play an active role in cyclosporin A nephrotoxicity and demonstrates that the concomitant administration of nifedipine to rats with reduced renal mass does not ameliorate cyclosporin A-induced renal impairment.


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