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Biomedical subjects

L B Travis

Publications and source records attributed to L B Travis.

At least 127 records · Page 7Linked to original sources
PubMed1977

Nephronophthisis. Renal function and histologic studies in a family.

Nephronophthisis (previously described as familial juvenile nephronophthisis and medullary cystic disease) is characterized by insidious renal failure, its main features being increased urinary sodium loss, pitressin-resistant hypotomic polyuria, polydipsia, normal urine sediment and absence of hypertension. Renal function and histologic studies were performed in a family in which two siblings had this disorder, while the parents and two other siblings appeared clinically normal. Both parents demonstrated a moderate impairment of maximum urinary concentration. The values for tubular free water reabsorption (TcH2O) were relativley normal in the parents and the healthy siblings. One of the index patients showed only minimal sodium wasting even though he had hyposthenuria, thus suggesting an involvement of the collecting ducts in the early stage of neophronophthisis. No evidence of proximal tubular dysfunction was found. Although the light-microscopic examination of renal biopsies from the parents and the healthy siblings was unremarkable, electron microscopy revealed probable abnormalities in all four. An autosomal recessive mode of inheritance is, therefore, suggested in this family. The etiology of nephronophthisis is obscure but a likely possibility is that the renal damage results from an inborn metabolic error.

Adolescent↗
PubMed1977

The mechanism of urinary concentration in nephrogenic diabetes insipidus.

The authors have evaluated urinary adenosine 3',5'-monophosphate (cyclic AMP) excretion and renal function during Pitressin administration, hypertonic saline administration, and water deprivation in two siblings with vasopressin-resistant diabetes insipidus and in normal control subjects. After vasopressin administration normal subjects experienced a 2-fold rise in urinary cyclic AMP excretion from 3.2 +/- 0.7 to 5.6 +/- 1.3 nmol/min (P less than 0.001) whereas cyclic AMP excretion was unchanged in both patients (patient AC 4.4 +/- 0.9 to 4.3 +/- 2.1; patient TC 2.2 +/- 0.9 to 2.6 +/- 0.9 nmol/min) with nephrogenic diabetes insipidus (NDI). Urinary cyclic AMP excretion was measured during infusion of 2.5% saline, after vasopressim administration, and after water deprivation. Cyclic AMP excretion was not different from control values in the NDI patients during any of the experimental conditions. Furthermore, there was no difference in cyclic AMP excretion when periods of dilute urine excretion (patient AC 4.5 +/- 1.1; patient TC 2.1 +/- 0.8 nmol/min) were compared with periods when urine concentration was greater than that of plasma (AC 3.5 +/- 1.3; TC 1.8 +/- 0.9 nmol/min). Both subjects responded to parathyroid hormone infusion with a 2-fold increase in urinary cyclic AMP excretion. Excretion of concentrated urine was paralleled by a marked decrease in urine flow to less than 1 ml/min/m2. During periods of hypotonic urine excretion (Uosm/Posm less than 1.0) average glomerular filtration rate (GFR) in patient AC was 67.0 +/- 3.0 ml/minm2 whereas in patient TC it was 70.1 +/- 8.1 ml/min/m2. When each patient was excreting a hypertonic urine (Uosm/Posm greater than 1.0) after fluid deprivation their GFR had decreased significantly (P = 0.001) to 31.6 +/- 8.9 and 33.3 +/- 10.3 ml/min/m2, respectively. Ability of these two subjects with NDI to concentrate their urine to Uosm/Posm greater than 1.0 in the absence of an increase in urinary cyclic AMP but associated with a decrease in GFR to 50% normal indicates that urinary concentration was effected by a reduction in GFR rather than a partial response to antidiuretic hormone (ADH). Their ability to concentrate their urine during periods of modest volume depletion would protect them from progressing to more severe stages of dehydration and result in the relatively benign course of their disease. It is feasible that in patients previously reported to have had clinically "partial" NDI this mechanism may have been operative.

Adolescent↗
PubMed1977

Toxic psychosis due to cyproheptadine in a child on hemodialysis: a case report.

In 1971 Simmons et al. presented evidence that children receiving regular dialysis therapy required approximately seventy percent of recommended caloric intake to achieve normal growth. Since that time, pediatric nephrologists and dietitians have strived to meet that requirement. In an effort to attain adequate caloric intake, cyproheptadine, a known appetite stimulant, was prescribed to a child on chronic hemodialysis. The following reports the unexpected complication of toxic psychosis that resulted.

Child↗
PubMed1977

Simultaneous iothalamate, creatinine, and urea clearances in children with renal disease.

Glomerular filtration rate (GFR) is often used to evaluate and manage patients with renal disease. Few studies in children have compared accurate estimations of GFR (clearance of inulin and/or iothalamate) with the clearance of creatinine which, because of simplicity, has been used as an approximation of GFR. At reduced levels of GFR, studies in adults suggest that the mean of the creatinine and urea clearances closely approximate the GFR. The present investigation shows that the clearance of creatinine approximates the GFR at normal levels; however, at reduced levels the creatinine clearance and the mean of the creatinine and urea clearances both overestimate the GFR as measured by iothalamate. The clearance of creatinine remains a useful clinical tool if its limitations at low levels of GFR are realized.

Adolescent↗
PubMed1976

IgA nephropathy in children.

Three children presented with proteinuria, microscopic hematuria, episodic gross hematuria and normal renal function. Renal histology consisted predominantly of mesangial IgA deposition. The above clinical and biopsy findings are consistent with a diagnosis of IgA nephropathy. To date, these 3 children have maintained normal renal function. The authors hypothesize that this may be due to the absence of simultaneous complement deposition within the glomerulus.

Child↗
PubMed1975

Urinary lactic dehydrogenase isoenzyme 5 in the differential diagnosis of kidney and bladder infections.

Urinary lactic dehydrogenase (U-LDH) isoenzyme assays were performed on ch2) as well as normal controls (N = 24). Docuemntation of bladder and kidney infection was accomplished by means of the bladder washout test, culture of ureteric urine (in patients with urinary diversion), kidney function studies including the maximal urine concentration test, clinical symptomatology and radiologic appearance of the urinary tract. Total U-LDH in normal children (10.8 +/- 1 mU/ml) was lower than in patients with bladder (27.0 +/- 3.9 mU/ml) or kidney (226 +/- 67.3 mU/ml) infections (P less than 0.005). In normal children isoenzymes 1 and 2 predominated (LDH-1 migrates fastest to anode -- fast zone pattern). In patients with bladder infections, the isoenzyme patterns varied but the concentration of isoenzyme 5 (3.1 +/- 0.8 mU/ml) was lower (P less than 0.005) than in patients with kidney infections (120 +/- 39 mU/ml). In the latter, isoenzymes 4 and 5 predominated (slow zone pattern). Since overlap between kidney and bladder infections regarding isoenzyme 5 concentrations (at 3 SD) occurred in only one individual (patient 37), a correct differential diagnosis using U-LDH-5 alone would have been possible in 94% of the children with pyelonephritis or 97% of the total patient population (kidney + bladder).

Adolescent↗