Search

Problems of fecal elimination are commonly encountered by the pediatric urologist and surgeon. The Malone antegrade continence enema has been described as a means to administer a large volume enema via a continent catheterizable appendicocecostomy, resulting in reliable fecal elimination. Of 22 patients undergoing this procedure 16 reported total continence 4 months or longer after surgery. Complications are relatively minor and tap water appears to be a safe solution for the antegrade continence enema. A nonrefluxing, imbricated appendicocecostomy is preferable to prevent cutaneous fecal or gas leaks.

We examined the properties of Na+/K+/2Cl- cotransport in cultured mouse mTAL cells with respect to its kinetics, the contribution of K/K exchange to K fluxes mediated by the cotransporter, and [3H]bumetanide binding and turnover numbers in media with varying osmolality. The addition of bumetanide, the replacement of external Na+ or the replacement of external Cl- resulted in an almost identical (approx. 50%) decrease in K+ influx, suggesting that Na(+)-dependent, Cl(-)-dependent, BS K+ influx was a measure of Na+/K+/2Cl- cotransport. The kinetics of the BS K+ influx revealed a high affinity for external Na+ (apparent Km 7 mM) and external K+ (apparent Km 1.3 mM), but a very low affinity for external Cl- (apparent Km 67 mM with a two-site model). Of interest was the finding that none of the K+ (86Rb+) efflux was sensitive to bumetanide, suggesting the absence of cotransport mediated K/K exchange in this cell type. Specific [3H]bumetanide binding was a saturable function of free bumetanide concentration with a Kd of 0.20 microM and maximum binding (Bmax) of 0.63 pmol/mg, or about 53,000 sites per cell. Simultaneous transport and bumetanide binding assays yielded a turnover number of 255 min-1. The omission of external Na+, K+ or Cl- reduced specific [3H]bumetanide binding to values indistinguishable from zero. Changing medium osmolarity resulted in a co-ordinate change in BS K+ influx and bumetanide binding, with a monotonic increase in both transport and bumetanide binding with increase in osmolality from 200 to 400 mosmol/kg. About 85% of the cotransporter sites were located on the apical side, as in the intact mTAL tubule. The simultaneous measurement of BS ion transport and [3H]bumetanide binding in the mTAL cell may provide valuable insights into the regulation of Na+/K+/2Cl- cotransport in this nephron segment.

The long-term effects of extracorporeal shock wave lithotripsy (ESWL*) on children treated for renal calculi are unclear. To study the long-term bio-effects of this mode of treatment on the immature animal we evaluated 30 New Zealand white rabbits at 7 weeks of age for weight, serum blood urea nitrogen and creatinine, and arterial blood pressure after which they underwent left nephrectomy. Each group of 5 rabbits received ESWL of varying levels (500 to 3,000 shock waves) to the remaining right kidney using the Northgate SD3 lithotriptor (spark gap mediated). One control group received no shock waves. At maturity (16 weeks) the aforementioned parameters were measured again, and the kidneys and any grossly abnormal adjacent organs were examined. We found no significant change in total animal growth, renal growth, renal function or perirenal organs in the post-ESWL groups versus the control group. All post-ESWL groups had an increase in mean arterial blood pressure versus the control group with 3 of 6 groups showing significant increases (p less than 0.05). Histological renal changes, seen at all energy levels of ESWL delivered, included interstitial fibrosis, tubular atrophy, glomeruli destruction, capsular thickening, perivascular fibrosis and mild arteriole wall thickening. Changes were proportional to the number of shocks received. We conclude that ESWL delivered to immature animals does not significantly affect renal growth and function but it can cause significant permanent histological renal changes even at low doses and may result in an increase in adult mean arterial blood pressure.

In a group of 18 male patients with spinal cord injury, we found serum creatinine to be within normal limits or only minimally elevated despite significant reduction in creatinine clearance. In 8 control subjects with serum creatinine between 1.0 and 1.5 mg/dL (88.4 and 132.6 mumol/L), the measured creatinine clearance was 66.4 +/- 28.2 mL/min. In contrast, in the 5 patients with spinal cord injury whose serum creatinine was in the same range, the measured creatinine clearance was only 31.0 +/- 19 mL/min. Urinary creatinine excretion was lower in patients with spinal cord injury than in the 18 male controls (653 mg/24 hr vs. 1505 mg/24 hr). The decreased urinary creatinine could not be explained by differences in age, sex, or body weight. We calculated the relationship of creatinine clearance (Ccr) and serum creatinine (Scr) in patients with spinal cord injury to be given by the equation Ccr (mL/min) = 45/Scr (mg/dL), r = 0.73. We recommend timed urine collections for creatinine to estimate creatinine clearance accurately for clinical evaluation of patients with spinal cord injury.

The distribution of a short-term potassium load was quantitated in three groups of acutely nephrectomized rats infused with KCl at 0.75, 1.50, and 2.25 mEq/kg/hr for 90 minutes. The rate of net potassium transfer from the extracellular fluid compartment to the intracellular fluid compartment was stable from 30 to 90 minutes and proportional to the rate of infusion, with no evidence of saturation of transport mechanisms. In the period 60 to 90 minutes, the calculated increments in intracellular potassium concentration over 10-minute intervals were similar to the respective increments in extracellular potassium concentration. The apparent volume of distribution of the infused potassium over this period was similar to total body water. At the termination of the infusions, the net potassium transfer rates rapidly fell to very low levels. Our studies support the view that the extrarenal modulation of short-term potassium load is dependent on changes in plasma potassium concentration that conform to a first-order linear kinetic model. The infusion of the selective beta 2-adrenergic blocker butoxamine without potassium administration to acutely nephrectomized rats resulted in a net efflux of potassium from the intracellular fluid compartment. The addition of butoxamine to three groups of rats receiving KCl at the previous rates resulted in a fixed decrement in net potassium transfer to the intracellular fluid compartment that was not significantly different from the net efflux of potassium seen with butoxamine alone. Despite beta blockade, the net transfer of potassium remained proportional to the infusion rate. Thus, in our studies, beta 2-adrenergic blockade had a relatively fixed influence on decreasing net potassium transfer, both under basal conditions and during short-term potassium administration.

Nine patients on maintenance haemodialysis with frequent muscle cramps were given 320 mg quinine sulphate or placebo (in an identical gelatin capsule) at the beginning of each dialysis for a period of 12 weeks. The frequency of cramps was significantly reduced during dialysis in patients receiving quinine sulphate. None of the haematological, auditory, or visual disturbances ascribed to quinine sulphate were noted.