[Physiopathology and treatment of metabolic changes in transintestinal urinary diversions]. / Fisiopatología y tratamiento de las alteraciones metabólicas en las derivaciones urinarias transintestinales.

The use of intestinal segments in the urinary tract can cause metabolic changes that depend on the intestinal segment utilized. The severity of these changes basically depends on the area of the intestinal mucosa in contact with urine, the duration of exposure to urine and renal function. The length of time the intestinal mucosa is in contact with urine largely depends on the surgical technique employed. It is longer for the reservoirs, intestinal neobladders and ureterosigmoidostomies than for the intestinal conduits with cutaneous urinary diversion and therefore carry a higher incidence of metabolic changes. Jejunal urinary diversion causes metabolic acidosis with hypochloremia, hyponatremia, hyperpotassemia, azotemia and dehydration in at least 50% of the cases. Ileal and colonic urinary diversion can cause metabolic acidosis, although the incidence is significantly less. Acidosis presents with hyperchloremia, hyperammonemia, hypersulfatemia, increased osmolality and uremia with normal creatininemia and a tendency to develop hypocalcemia, hypophosphoremia and hypomagnesemia. Recent studies performed in our service show that acidosis is basically due to the secretion of sodium bicarbonate by the intestinal segment used in the urinary tract, which causes water-salt depletion that is compensated by secondary hyperaldosteronism. Mild chronic acidosis is neutralized via the respiratory system and by the bone buffers, which leads to bone remodelling manifested by the significant increase of serum alkaline phosphatase levels and increased calciuria. These calcium phosphate changes, although statistically significant, do not appear to be important since they were not accompanied by changes of serum PTH levels, 25 and 1-25-cholecalciferol. Nicotinic acid as inhibitor of cyclic AMP synthesis failed to correct metabolic acidosis in the patients with transileal diversion.

Renal tubular acidosis in recurrent renal stone formers.

Renal tubular acidosis (RTA) is a well-known metabolic disturbance that may promote recurrent renal stone formation. However, its incidence, screening criteria and association with other lithogenic metabolic abnormalities are not established in recurrent nephrolithiasis. 10 of 50 consecutive recurrent renal stone formers had a persistent fasting morning urinary pH above 6.0 and/or a basal plasma bicarbonate concentration below 20.0 mM. Acid and alkaline loads disclosed RTA in 3 patients: 1 patient had incomplete type-1 distal RTA in addition to hyperoxaluria; a second patient showed complete type-2 proximal RTA, hyperoxaluria and renal hypercaliuria; and a third patient had incomplete proximal RTA without any other metabolic derangement. These results reinforce the importance of RTA as an isolated metabolic abnormality among recurrent renal stone formers. In addition, RTA appears to be more commonly associated with other lithogenic metabolic derangements than has been previously suspected. The extensive metabolic protocol used in this study provides a useful tool in the diagnosis and therapeutic considerations of recurrent nephrolithiasis.

[Tubular function and renal acidifying in juvenile diabetes mellitus of short evolution]. / Estudio de la función tubular y capacidad renal de acidificación en la diabetes mellitus infanto-juvenil de corta evolución.

The fractional excretion of uric acid, calcium, phosphorus, magnesium and other ions, and the urinary acidifying capacity were studied in then patients with juvenile diabetes of short evolution and in a control group matched for age, sex, and body surface. The diabetic patients showed a hyperexcretion of uric acid, sodium, potassium, chloride and ammonium which was unrelated to the increment of glomerular filtration rate or to glucosuria, and could not be ascribed to diet. The pathophysiologic interpretation of these findings is discussed, concluding that they might be the result of an increase in the filtered load and the behaviour of the tubules in front of the glomerular hyperfunction or metabolic disturbance inherent to the diabetic condition.