Assessment of divided renal function by renography. Validation in patients with separate urine collections from each kidney.

Divided renal function was measured by 99mTc-DTPA renography using a gamma camera and a computer-assisted program. In 14 patients with permanent bilateral ureterostomies (7) or temporary ureteric catheterization (7), split renal function was calculated by analysis of the initial phase of the kidney activity-time curve and measured simultaneously by conventional clearance techniques. A high correlation was found between individual clearances measured by computation and by the conventional procedure. The correlation coefficient between the results obtained by the two techniques was 0.94 (P less than 0.001). A high correlation was also shown to exist between the computed clearance and the renal uptake of mercury after administration of 197HgCl. It is concluded that 99mTc-DTPA is particularly useful for the measurement of divided renal function without the need for urine collection.

Increased renal excretion of 3 hydroxyproline in patients with active glomerular nephropathies and with polycystic renal disease.

The renal excretion of 3 hydroxyproline (3 HYP) and 4 hydroxyproline (4 HYP) was investigated in control subjects and in patients with various renal diseases. In normal adult subjects urinary 3 HYP was 12.5 +/- 3.5 (SD) mumoles/24 hr, 4 HYP was 226 +/- 62 mumoles/24 hr and the percentage ratio 3 HYP/4 HYP 5.4 +/- 0.5. This ratio was reduced during growth because of a relative excess of 4 HYP. In patients with acute glomerular disease (n = 12) 3 HYP was increased to 17.1 +/- 5.8 mumoles/24 hr (P less than 0.01), and the ratio 3 HYP/4 HYP was 7.3 +/- 0.7% (P less than 0.01). Such an increase in 3 HYP was not observed in patients with chronic glomerulonephritis (n = 24) where 3 HYP was 9.6 +/- 5.0 mumoles/24 hr and 3 HYP/4 HYP 5.7 +/- 1.6% or with diabetic glomerulopathy (n = 6). In patients with chronic interstitial nephritis (n = 8) the 3 HYP/4 HYP ratio was decreased except in patients with polycystic renal disease (PKD) where it was increased (P less than 0.001). The daily urinary content of 3 HYP and 4 HYP was slightly altered by renal insufficiency. Urinary 3 HYP did not change significantly in patients with GN with the nephrotic syndrome whatever the histological lesion. These results indicate that urinary 3 HYP: 1) is increased when glomerulonephritis is clinically acute or subacute; 2) is increased in PKD whatever the level of renal insufficiency.

Effect of acute ethanol loading on parathyroid gland secretion in the rat.

Acute ethanol loading in the rat induces hypocalcemia and hypermagnesemia. In addition, hypocalcemia is not corrected by exogenous PTH. In the rat the mechanism of these changes was investigated by measuring plasma immunoreactive parathyroid hormone (PTH). PTH was also measured in culture medium in which parathyroid glands were incubated. The addition of ethanol to test tubes did not interfere with PTH measurement. Absolute ethyl alcohol diluted to 50% with distilled water was administered via an intragastric tube. It failed to induce an increase in plasma immunoreactive PTH level. Similarly, it prevented an increase in plasma PTH after disodium EDTA injection. Thus in the presence of ethyl alcohol plasma PTH failed to increase in spite of a significant decrease of plasma calcium. In vitro studies showed that the decrease of calcium concentration of the medium from 1.50 to 0.75 mmol/l was associated with a 3 to 5 times increase in PTH secretion rate. This increase was suppressed when ethanol was added to the culture medium. In conclusion, ethanol loading via gastric tubing induced: 1) decrease in plasma calcium; 2) suppression of immunoreactive PTH secretion in the presence of hypocalcemia. It is postulated that the acute hypocalcemic effect of ethanol loading is mediated by a dual effect at the level of the bone and the parathyroid gland.

[Hemorrhagic fever with renal syndrome due to Hantaan virus or a serologically related virus]. / Fièvre hémorragique avec syndrome rénal due au virus Hantaan ou à un virus sérologiquement apparenté.

Seven cases of acute renal failure consecutive to haemorrhagic fever with renal syndrome (HFRS) due to the Hantaan virus or to a serologically related virus are reported. These cases were observed in north-eastern France between March, 1983 and January, 1984. All patients were of rural origin and had been in contact with field mice. The predominant initial clinical symptoms were signs of infection and diffuse muscle pain, without evidence of haemorrhage. However, massive proteinuria was noted, and acute anuric renal failure unaccompanied by oedema or arterial hypertension developed. Renal biopsy performed in 2 patients showed tubular and interstitial nephritis but no glomerular or vascular lesions. Two patients only required haemodialysis. All patients recovered within 2 to 8 weeks without sequelae. Antibodies directed against the Hantaan virus were detected by indirect immunofluorescence tests, and seroconversion could be demonstrated in 2 patients seen at a sufficiently early stage. The risk of epidemics suggested by this small outbreak of HFRS can only be evaluated after an exhaustive epidemiological study.

Urinary 3-hydroxyproline in renal disease.

The renal excretion of 3-hydroxyproline (3-HYP), an isomer of 4-hydroxyproline (4-HYP) found 6-10 times more in basement membrane collagen than in interstitial collagen, was investigated in control subjects and in 58 adult patients with various kidney diseases. With the exception of polykystic renal disease, all the nephropathies were investigated by renal biopsy. In normal adult subjects urinary 3-HYP was 12.5 +/- 3.5 (SD) mumol/24 h, 4-HYP 226 +/- 62 mumol/24 h and the percentage ratio 3-HYP/4-HYP 5.5 +/- 0.5. This ratio was twice as little during growth because of a relative excess of 4-HYP. In patients with acute glomerular disease (acute and subacute glomerulonephritis, lupus nephritis...) (n = 13) 3-HYP was 17.1 +/- 5.8 mumol/24 h (p less than 0.01 when compared with the normal) and 4-HYP 234 +/- 77 mumol/24 h. The ratio between the two values was 7.3 +/- 0.7 (p less than 0.001). Such an increase in 3-HYP was not observed in patients with chronic glomerulonephritis (n = 24) where 3-HYP was 9.6 +/- 5.7 mumol/24 h and 3-HYP/4-HYP 6.0 +/- 1.6, neither in patients with diabetic glomerulonephritis (n = 6). In chronic interstitial nephritis (n = 8) the 3-HYP/4-HYP ratio was decreased with the exception of polykystic renal diseases (PKD), where it was increased (p less than 0.001). The daily urinary contents of 3-HYP and 4-HYP were slightly altered by renal insufficiency. In glomerulonephritis with nephrotic syndrome whatever the histological lesions, urinary 3-HYP did not change significantly. These preliminary results indicate that urinary 3-HYP (1) is increased when glomerulonephritis is clinically acute or subacute; (2) is increased in PKD suggesting a possible inborn error of collagen metabolism.

[Role of sodium in the control of compartmental distribution of water during hemodialysis. I. Measurement of water transfer]. / Rôle du sodium dans le contrôle de la répartition compartimentale de l'eau en hémodialyse. I.--Measure des transferts d'eau.

Symptomatic hypotension and other symptoms of the so-called dialytic desiquilibrium syndrome have been related to alterations of body fluid osmolality and distribution. Fluid removal from the intracellular compartment can be achieved by manipulating the sodium dialysate (NaD). The extracellular fluid volume ( EFCV ) was measured with inulin and/or 35SO = 4. Total body water changes were calculated in terms of fluid substraction induced by dialysis. They were monitored in 12 patients on hemodialysis with a highly permeable membrane and a careful monitoring of ultrafiltration. NaD was maintained constant throughout the session and was comprised between 140 and 170 mmol/l. Below 150 mmol/l NaD, ECFV was reduced more than the weight loss, indicating concomitant intracellular water loading. Conversely, over 150 mmol/l NaD weight loss resulted from extracellular and cellular water. We conclude: 1) transcellular water shift during dialysis is dependent of sodium dialysate; 2) net cellular water-shift was obtained for NaD higher than 150 mmol/l; 3) at least two compartments for water distribution should be taken into account for sodium modeling.

Long-term results of dialysis therapy with a highly permeable membrane.

A five-year study of short-term dialysis using highly permeable polyacrylonitrile membrane AN 69 was started in March 1973 to compare the effects of AN 69 and Cuprophan membrane (CM). The time of dialysis was calculated for each patient on the basis of vitamin B12 clearance of the dialyzer and the residual glomerular filtration rate. For the study, 101 patients (38,555 dialysis sessions) who had been dialyzed for more than six months were selected. They were divided into three groups: Group I (n = 31) patients treated with AN 69 only; Group II (n = 31) patients treated with CM; Group III (n = 39) patients treated first with the CM and then with AN 69. Patients treated with AN 69 had higher levels of plasma urea but no particular metabolic disturbances were observed. The dialysis sessions were significantly better tolerated with AN 69 than with CM, however, the main advantage of using AN 69 is the shortening of dialysis time. The duration of dialysis was 9.5 +/- 0.2 hours per week with AN 69 and 16.4 +/- 0.2 hours per week with CM. Shortening of dialysis time permits better social rehabilitation of the patients. The shorter dialysis was not associated with any recognizable side effects that could be demonstrated by routine clinical and biological analysis.

[De novo purine biosynthesis. In vitro measurement in hyperuricemia (author's transl)]. / Mesure de la biosynthèse de novo des bases puriques dans les hyperuricémies.

De novo purine biosynthesis has been investigated in circulating blood lymphocytes in vitro. N-formyl-glycinamide ribonucleotide (FGAR) has been mesured using 14C-formate incorporation in the presence of azaserine, a metabolic inhibitor blocking the metabolical pathway at the level of FGAR synthesis. Such a synthesis was measured in 20 healthy controls, 24 patients with primary gout (11 on allopurinol therapy) and 26 patients with chronic renal failure and secondary hyperuricemia (8 on allopurinol therapy). Among gouty patients without allopurinol therapy, FGAR synthesis was normal in 5 and increased in the others. FGAR synthesis was decreased in patients with renal failure whatever the therapy. However, FGAR synthesis remained increased in patients with a primary gout complicated with renal insufficiency. The test we propose for de novo purine biosynthesis measurement is simple and of value to analyse the patho-physiology of hyperuricemia and its therapy. The test allows an acurate discrimination between primary and secondary hyperuricemia in the presence of renal insufficiency.

[Acute renal failure caused by clometacin hypersensitivity]. / Insuffisance rénale aiguë par hypersensibilité à la clométacine.

Renal involvement is not frequently observed during therapy with clometacine and its mechanism not fully understood. We report on a case of acute renal failure occurring four times in conjunction with acute hepatitis before the causative effect of clometacine was demonstrated. Drug hypersensitivity was documented by anatomical findings consisting in renal interstitial infiltration by mononuclear cells and eosinophils and by hypereosinophilia, increase in plasma IgE and a positive basophil degranulation test.