[Prolonged acute renal failure and severe polyradiculopathy in ethylene glycol intoxication]. / Fracaso renal agudo prolongado y polirradiculopatía severa en paciente intoxicado con etilenglicol.

Ethylene glycol intoxication involves acute renal failure and severe metabolic acidosis. Prolonged renal insufficiency can occur but terminal chronic renal failure has been reported in very few cases. We describe a patient who after ingestion of 920 ml of ethylene glycol developed prolonged acute renal failure needing hemodialysis for 37 days and then he partly recovered renal function. The patient developed a severe sensitive-motor and autonomic polyradiculopathy.

Renal cortical intermediary metabolism in the recovery phase of postischemic acute renal failure in the dog.

Renal metabolism has been studied in eight dogs before and 48 hr after a 60-min period of renal ischemia induced by clamping the left renal artery with the simultaneous removal of the right kidney, and in 12 sham-operated animals. The study involved the measurement of renal uptake and production of lactate, glutamine, glutamate, alanine, ammonium, and oxygen, and the measurement of the tissue concentrations of ATP, glutamine, lactate, alpha-ketoglutarate, aspartate, and alanine in the renal cortex. Two days after a temporary renal ischemia, the remaining kidney showed a 22% decrease in glomerular filtration rate (GFR) and a 25% decrease in renal plasma flow. Fractional sodium and potassium excretions were similar to those of control dogs. Renal production or extraction of glutamine, glutamate, alanine, ammonium, and oxygen (all expressed by 100 ml of GFR) was not significantly different in basal conditions or 2 days after ischemia, but lactate extraction was reduced in postischemic kidneys (-101 +/- 29 vs -204 +/- 38 mumol/100 ml GFR in control dogs). The cortical concentrations of glutamine and glutamate were lower in postischemic than in control kidneys. No differences were found in cortical concentration of alpha-ketoglutarate, aspartate, lactate, pyruvate, or ATP, but total nucleotides and inorganic phosphate were decreased in postischemic kidneys. It is concluded that in the recovery phase of the ischemia, a decreased lactate uptake is the main metabolic change, and total ATP production is adapted to the decrease of GFR and sodium reabsorption.

Interleukin 2 production in a family with systemic lupus erythematosus and a C4Q0 heterozygous inheritance.

Interleukin 2 production was studied in a family with systemic lupus erythematosus (SLE) and a C4Q0 heterozygous inheritance. Autoimmune manifestations seemed to be associated with the HLA haplotype containing the C4Q0 allele, which was shared by all four ill family members. Concentrations of interleukin 2, however, did not associate either with the haplotype or with the clinical or serological manifestations, as diminished concentrations of interleukin 2 were found in only two subjects with SLE. Thus the defect in this family seemed to be acquired rather than genetically conditioned.

Intermediary metabolism in renal proximal tubules in the recovery phase of experimental renal ischemia in dogs.

Intermediary metabolism has been studied in a viable suspension of renal proximal tubules isolated from dogs before and after 48 h of a 60 min period of renal ischemia by clamping the renal artery. The study consisted in measurements of tubular uptake/production of glucose, lactate, glutamine, glutamate, alpha-ketoglutarate, alanine, ammonium, and oxygen, using as substrates either glutamine 1 or 5 mM (+ glutamate 0.1 or 0.5 mM) or lactate 1 or 5 mM (+ pyruvate 0.1 or 0.5 mM). The combination of glutamine + lactate was also studied. Data revealed that the gluconeogenic ability of the postischemic tubules was maintained, with the exception of glutamine 5 mM as substrate (8.5 +/- 2.1 vs 15.4 +/- 2.1 mumol/min/g in control tubules). The production of NH4 was also decreased only with this substrate (from 214 +/- 15 to 165 +/- 9 mumol/min/g). Lactate extraction was decreased in the postischemic tubules, but the difference was only significant when lactate + glutamine 1 mM was used as substrate (72 +/- 12 vs 44 +/- 6 mumol/g/min). Postischemic tubules showed a greater oxygen consumption when either glutamine or lactate 1 mM were used, but lower ouabain-inhibitable O2 consumption when these substrates were used at 5 mM. These data revealed a modification of the metabolic profile of proximal tubules during the recovery of transient renal ischemia.

Renal ammoniagenesis during the recovery phase of postischemic acute renal failure in the dog.

Renal ammoniagenesis has been studied in 6 dogs before and 48 h after a 60-min period of renal ischemia induced by clamping the renal artery and in 6 sham-operated animals. Two days after temporary renal ischemia, the dogs showed a 25% decrease in glomerular filtration rate and renal plasma flow and a similar decrease in sodium reabsorption. Renal production of ammonium was not significantly different under basal conditions or 2 days after ischemia, but more ammonia was released by the urine in the postischemic dogs. Renal uptake of glutamine was similar in control and in postischemic kidneys. It is concluded that during the recovery phase of the ischemia, renal ammoniagenesis is conserved.

[Nephronophthisis: study of 10 cases. Incidence, natural history and associated pathology (author's transl)]. / Nefronoptisis: análisis de 10 casos. Incidencia, historia natural y patología asociada.

Nephronophthisis is a chronic interstitial nephropathy which in childhood may lead to terminal renal failure. Between January 1975 and July 1980, 41 children with terminal renal failure were seen in our service, of which 10 (21.9%) presented with nephronophthisis. Age of the patients ranged from 3.5-18 years, boys were in the majority (8/2). Three cases were isolated and 7 were familial (3 families). Onset was during the first year of life in 8 patients, and polydipsia-polyuria were the first symptoms. Retarded growth and anemia proportionate to the degree of renal failure were present in all patients. When diagnosed, 5 patients (50%) presented terminal renal failure, and the other 5 had renal failure of different degrees. Moderate proteinuria was found in 4 patients, without changes in urine sediment. Sodium depletion in urine was high in 5 cases and maximal urine osmolarity was less than 500 muOsm/l after hydropenia in all cases. Four had associated mental deficiency with cerebellar ataxia associated in two and congenital hepatic fibrosis (confirmed histologically) in one. The diagnosis was confirmed by biopsy in 8 and in two of these on frozen section during nephrectomy prior to kidney transplantation. At present, five of the patients are in maintenance hemodialysis, two died at home due to cardiovascular complications in terminal renal insufficiency and the remaining ones presented different degrees of renal insufficiency. Time elapsed between onset of the symptoms and inclusion in hemodialysis or death ranges form 6 months to 13 years (mean 6.7 years).

Dynamics of ascites formation in rats with experimental cirrhosis.

Renal function, sodium balance, and ascites formation were observed during induction in rats of experimental cirrhosis. The same variables were studied after partial removal of the ascites in rats with experimental cirrhosis. Glomerular filtration rate (GFR) and effective renal plasma flow (RPF) did not change during hepatic cirrhosis development. Positive sodium balance significantly higher than that observed in controls preceded the appearance of ascites for a period of about 2 wk. When the ascites was removed, GFR, RPF and positive Na balance did not change if Na intake remained constant. Ascites reformation rate was largely dependent on sodium balance. These data strongly support the "overflow" theory of ascites formation and are difficult to reconcile with the classical "underfilling" theory.

Sodium excretion after bilateral adrenalectomy in rats with experimental cirrhosis.

Bilateral adrenalectomy (ADX) or a sham procedure was performed in cirrhotic and control rats. After ADX, controls increased their sodium excretion with respect to the basal values but cirrhotics did not. When sodium-loaded, the ADX cirrhotic rats retained a significant amount of the load. These data do not support a primary role of aldosterone in the impaired sodium handling by cirrhotic rats.

Effect of propranolol on glycerol induced acute renal failure in rats.

The effect produced by propranolol, administered for a prolonged period of time and in large doses, on renal function in rats has been studied, as well as the modifications induced by this treatment in an experimental model of acute renal failure, and the effects of a single dose of propranolol given 1 hour before provoking failure. Propranolol, administered chronically, causes sodium and water retention and increases creatinine clearance. Acute renal failure induced by glycerol in rats treated for 7 days with propranolol is less severe than the one produced in untreated animals. In this ARF model, a single dose of propranolol does not seem to have a protective effect.

A micropuncture study of salt and water retention in chronic experimental cirrhosis.

The object of this study was to localize increased sodium resorption in rats with chronic hepatic cirrhosis. Cirrhosis was induced by the administration of phenobarbital and carbon tetrachloride. The animals retained salt and water after loading and showed edema and ascites. Salt and water balance, clearance, and micropuncture tests were performed. Five or six weeks after the start of procedures to induce injury, the rats were unable to excrete salt and water loads promptly. Urine flow and sodium concentration were significantly less in cirrhotic rats with edema and ascites than in the normal controls. The glomerular filtration rate was slightly lower in the right, nonmicropunctured kidney but was the same in the left. The nephron glomerular filtration rates of surface nephrons were equal in both the experimental and control rats. The fractional proximal resorption rate was notably greater in cirrhotic rats, as was the total proximal nephron resorption rate. That increased proximal resorption alone might account for diminished sodium and water excretion cannot be demonstrated from this study, although we believe that major evidence is provided of the importance of proximal resorption in this phenomenon.

[Tubular permeability maintained in post-ischemic acute renal failure (author's transl)]. / Permeabilidad tubular conservada en la insuficiencia renal aguda postisquémica

The effect of nearly total renal ischemia during a two hour period on glomerular filtration and urine composition was studied in relation to tubular permeability and tubular obstruction, two mechanisms that could explain renal insuficiency after iscehmia. Studies on creatinine clearance, micropuncture and microinjection of 14C-inulin into the proximal tubules by means of a hydraulic system were performed before and after the period of ischemia. Thirty minutes after the withdrawal of arterial obstruction, the animals exhibited a maintained diuresis, 50 per cent reduction in glomerular filtration in the superficial nephrons and in the total kidney, a reduction in the proximal fractional absorption of water, and also an increase in the urinary elimination of sodium. The glomerular filtrate of cortical nephorns obtained by micropuncture in anterior areas of the proximal tubules did not differ significantly from the one obtained by micropuncture in more distal areas. The inulin injected into the proximal tubules of a kidney was entirely eliminated by it.