Child nephrology and urology最新文献

Urinary excretion of norepinephrine, epinephrine and dopamine was investigated in children with diabetic ketoacidosis. Besides pronounced hyperglycemia and metabolic acidosis, severe hypovolemia was also observed. At the onset of the study, urinary excretion of norepinephrine, epinephrine and dopamine was markedly elevated. Fluid replacement decreased urinary catecholamine excretion. Norepinephrine: 996 +/- 97 vs. 253 +/- 29; dopamine: 5,108 +/- 480 vs. 3,175 +/- 715; epinephrine: 402 +/- 81 vs. 77 +/- 200 pmol/min/1.73 m2. During ketoacidosis, there was a significant negative correlation between urinary norepinephrine excretion and endogenous creatinine clearance. Urinary output of both norepinephrine and dopamine correlated significantly with diuresis, while sodium excretion only correlated with dopamine excretion. Our data suggest that in diabetic ketoacidosis increased urinary excretion of norepinephrine may participate in renal hypoperfusion and hypofiltration. Elevated renal dopamine production contributes to sodium loss, characteristic for diabetic ketoacidosis.

In 40 premature infants fed human milk with an actual gestational age of 261 +/- 16 days and an actual body weight of 1.06-2.75 kg, 44 urine samples were collected, and blood acid-base status was measured on day 32 (+/- 16) of life. In the urine, the following results (mean +/- SD) were obtained: urine pH 6.05 +/- 0.65, titratable acidity 0.24 +/- 0.14 mmol/kg/day, ammonium 0.78 +/- 0.25 mmol/kg/day, net acid excretion 0.83 +/- 0.47 mmol/kg/day. There was no significant correlation between renal net acid or ammonium excretion and actual body weight. However, urine pH was positively correlated with body weight. Obviously, premature infants with an actual body weight below 1.5 kg need a higher stimulation of renal hydrogen ion secretion to excrete the same amount of ammonium than those with an actual body weight of about 2.5 kg. The limited renal acidification capacity of very low birth weight infants is a risk factor for the development of late metabolic acidosis.

Hematuria has been noted to be a presenting symptom of urinary tuberculosis. In the last few decades because of the decreasing incidence of tuberculosis in the United States, the association of tuberculosis and hematuria has been neglected. Now that the incidence of tuberculosis is again on the rise, it is timely to remind the medical community of this association. We present 3 children with hematuria associated with positive tuberculin tests. Mycobacterium tuberculosis was cultured from the urine of one patient. Mycobacterium avium-intracellulare was cultured from a second patient. All 3 patients showed clearing of their hematuria with antituberculosis therapy. A tuberculin test should once again be considered part of the standard work-up of hematuria.

We describe our experience with chronic peritoneal dialysis in 17 infants. Fourteen boys and 3 girls, aged 2.7-22.5 months, were on continuous ambulatory peritoneal dialysis (CAPD) for 215.1 months with 5 infants on continuous cycling peritoneal dialysis (CCPD) for 71.2 months subsequently. Analysis of growth and biochemical data on 16 CAPD and 5 CCPD patients showed poor linear growth despite improved weight gain, high incidence of developmental delay, tendency to lower plasma albumin, phosphate and sodium and increased plasma cholesterol and triglyceride levels. Overall chronic peritoneal dialysis proved to be a possible and effective means of dialysis in infants.

An unusual case of severe hypercholesterolemia and hypertriglyceridemia is described in a child with nephrotic syndrome. The severe hyperlipidemia in this patient was most likely induced by multiple interacting factors which included the metabolic abnormalities of nephrotic syndrome, steroid therapy, the underlying genetic predisposition of ApoE-2 homozygosity as well as diet and diuretic therapy. The result of these factors was an extremely severe type III hyperlipoproteinemia. The pathogenesis of hyperlipidemia in this setting is discussed.

Twenty-three anemic children with end-stage renal failure (ESRD), aged 0.1-19.0 years (X +/- SD, 8.3 +/- 5.7 years), were treated with intravenous recombinant human erythropoietin (rHuEPO). Eleven were on conservative treatment and their estimated glomerular filtration rate (EGFR) was 11.8 +/- 3.8 ml/min/1.73 m2; 7 were on continuous ambulatory peritoneal dialysis (CAPD) and 5 on chronic hemodialysis. rHuEPO was given once a week in predialysis and CAPD children and thrice weekly in patients on hemodialysis. The initial dose of 50 U/kg/week was increased gradually up to a target hemoglobin of 10-12 g/dl. After 4.3 +/- 1.3 months of treatment, hemoglobin increased from 7.4 +/- 1.3 to 10.7 +/- 1.4 g/dl (p less than 0.001). An hemoglobin concentration of 11.4 +/- 0.9 g/dl was maintained with a rHuEPO dose of 289 +/- 86 U/kg/week. The response was similar in predialysis, CAPD, and hemodialysis children. No change in renal function was observed in predialysis children, EGFR being 11.8 +/- 3.8 and 10.8 +/- 1.7 ml/min/1.73 m2, before and after rHuEPO therapy. All children improved appetite, physical activity, and the sense of well-being. Four developed mild hypertension that was easily controlled with antihypertensive therapy. Heparin dose had to be increased during the hemodialysis sessions to avoid clotting of the filter. Serum calcium increased from 9.9 +/- 0.9 to 10.5 +/- 0.9 mg/dl (p less than 0.001). Serum aluminium levels also increased from 65 +/- 17 to 100 +/- 15 micrograms/l, p less than 0.01. A linear correlation (r = 0.58, p less than 0.01) between aluminium levels and rHuEPO dose was found.(ABSTRACT TRUNCATED AT 250 WORDS)

Immobilization hypercalcemia was initially described by Albright in 1941, and has most often been noted in adolescent males, presumably because their high rates of skeletal growth increase the likelihood that alterations in the equilibrium between bone deposition and resorption will have clinically apparent effects. The etiology of immobilization hypercalcemia is controversial, but is thought to result from normal levels of PTH acting with increased activity in the abnormal environment of immobilized bone. We describe a patient, immobilized following the resection of a large, locally invasive tumor, who developed hypercalcemia in conjunction with renal insufficiency and hypertension. The pathophysiology of immobilization hypercalcemia is discussed, as are the potential contributions of renal feedback mechanisms to the patient's hypertension and renal insufficiency.

Growth hormone (GH) influences a range of physiological functions, including renal plasma flow and glomerular filtration rate. Cells that secrete GH comprise a relatively large percentage of the total population of pituitary cells. The secretory activity of these cells is primarily regulated via peptide neurohormones from the hypothalamus. Direct influences of certain other factors have also been described. Human GH is present as a heterogeneous mixture of at least 20 molecular forms, most of which are 22,000 or 20,000 molecular weight monomers. Following release from the pituitary gland, GH circulates in either a 'free' form or bound to GH binding proteins. These binding proteins may have important effects on GH clearance and GH action at the level of the target tissue. The effects of GH are mediated, to a large extent, by insulin-like growth factors, formerly known as 'somatomedins'. The secretory pattern of GH is episodic, and occurs in bursts of varying frequency, amplitude, and duration. Changes in the pattern of GH secretion and its control occur with age. Recent data suggest that the specific characteristics of GH secretory bursts in humans are important to normal growth during childhood and adolescence.

Postbiopsy hematoma was assessed using ultrasonography in 106 infants and children (age 1 month to 15 years) who underwent a total of 122 percutaneous renal biopsies. Postbiopsy hematoma occurred in 22 (21%) of 105 successful biopsies. However, only 2 of these were symptomatic. Renal failure, mild and moderate hypertension and inexperience of the operator were not found to increase the incidence of postbiopsy hematoma in infants and children.

Two children, 1 with idiopathic nephrotic syndrome and 1 with endo-extracapillary glomerulonephritis, presented an episode of seizures and transient blindness at different times after i.v. pulse methylprednisolone (IVPMP) treatment. Neurological manifestations in patient 1 could be due to hypertension secondary to IVPMP, while the pathogenesis of such manifestations remained difficult to clarify in patient 2. The severity of uremia in patient 2 could be one of the conditions that, in association with the abrupt changes obtained with IVPMP, predispose to neurological manifestations. Careful clinical and biochemical monitoring seems necessary in children with primary glomerulonephritis, other than those transplanted, after IVPMP, and factors predisposing to neurologic sequelae should be further defined.