PubMed Health⌕ Search

Biomedical subjects

W Griswold

Publications and source records attributed to W Griswold.

18 recordsLinked to original sources
PubMed1998

Nonsteroidal anti-inflammatory drug use in adolescence.

Nonsteroidal anti-inflammatory drugs (NSAIDs) have been recently released as over-the-counter drugs making them more widely available to the general public. We present five cases of adolescents with complications, including acute and chronic renal failure, related to the use of NSAIDs. Risk factors for NSAID nephrotoxicity include chronic illness, dehydration, ethanol and use of other medications. Adolescents should be educated about the risks and prevention of NSAID toxicity.

Acute Kidney Injury↗
PubMed1997

Mutations in the chloride channel gene, CLCNKB, cause Bartter's syndrome type III.

Analysis of patients with inherited hypokalaemic alkalosis resulting from salt-wasting has proved fertile ground for identification of essential elements of renal salt homeostasis and blood-pressure regulation. We now demonstrate linkage of this phenotype to a segment of chromosome 1 containing the gene encoding a renal chloride channel, CLCNKB. Examination of this gene reveals loss-of-function mutations that impair renal chloride reabsorption in the thick ascending limb of Henle's loop. Mutations in seventeen kindreds have been identified, and they include large deletions and nonsense and missense mutations. Some of the deletions are shown to have arisen by unequal crossing over between CLCNKB and the nearby related gene, CLCNKA. Patients who harbour CLCNKB mutations are characterized by hypokalaemic alkalosis with salt-wasting, low blood pressure, normal magnesium and hyper- or normocalciuria; they define a distinct subset of patients with Bartter's syndrome in whom nephrocalcinosis is absent. These findings demonstrate the critical role of CLCNKB in renal salt reabsorption and blood-pressure homeostasis, and demonstrate the potential role of specific CLCNKB antagonists as diuretic antihypertensive agents.

Bartter Syndrome↗
PubMed1988

Colonic lesion expert system. Performance evaluation.

A computer-based expert system for diagnosing colonic sections as normal, adenoma or adenocarcinoma is described, along with an evaluation of its performance. On the basis of its knowledge base, consisting of the values of diagnostic clues and their associated certainty factors for the possible diagnoses, the system will suggest the diagnosis for new cases presented to it. Using the data provided for 16 diagnostic clues, the system arrived at correct diagnoses for all cases of normal colon, for 49 of 50 cases of adenoma and for 48 of 49 cases of adenocarcinoma. Sample outputs from the expert system are presented and discussed, and the effects of possible alterations in the data base are considered.

Adenocarcinoma↗
PubMed1985

Renal function in children after large dose contrast medium angiocardiography.

Serum creatinine and routine urinalysis were obtained and glomerular filtration rate estimated in 56 consecutive and hemodynamically stable children with congenital heart disease undergoing cardiac catheterization and angiocardiography, a day prior to, 1 and 7 days following the procedure. None had a history of renal disease. The patients were divided into 2 groups: Group I, 32 patients who received less than 3 ml/Kg of Renagrafin 60 and Group II, 24 patients who received greater than 3 ml/Kg. Despite a slight rise of creatinine on the first day, there were no statistically significant changes in serum creatinine or glomerular filtration rate for either group following the procedure. Occult blood was present in the urine of 2 in Group I and 1 in Group II prior to cardiac catheterization; this resolved in all cases after the procedure. Three patients in Group I and 1 in Group II developed transient trace proteinuria following the angiographic procedure. It is concluded that in children with congenital heart disease and normal kidney function, substantial doses of standard contrast medium administered during angiocardiography do not produce any apparent impairment of renal function.

Adolescent↗
PubMed1985

Proximal renal tubular acidosis in methylmalonic acidemia.

A patient with methylmalonic acidemia was found to have a persistent hyperchloremic acidosis. Investigation documented the presence of a proximal renal tubular acidosis. Between 14 and 18 months of age the urinary pH was as high as 8.0 when the serum bicarbonate was 17 mEq/liter and the threshold for bicarbonate was at 16-17 mEq/liter. When restudied at 33 months of age, the threshold had risen to 20 mEq/liter, but this was still abnormal and supplemental treatment was required to keep the serum concentration of bicarbonate above 20 mEq/liter. It is postulated that organic acid metabolites which accumulate in this and related disorders may interfere with renal tubular function as has been shown for maleic acid in experimental animals.

Acidosis, Renal Tubular↗
PubMed1982

Oral converting enzyme inhibitor in malignant hypertension.

Malignant hypertension, which developed in a 9-year-old boy after an episode of haemolytic uraemic syndrome, could not be controlled with antihypertensive agents. However, treatment with oral converting enzyme inhibitor (captopril) was effective in controlling the blood pressure and it averted bilateral nephrectomy. No adverse effects from the drug were noted.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1980

The cystic renal lesion in tuberous sclerosis.

A characteristic cystic renal lesion is described in three infants with tuberous sclerosis. Large cystic kidneys were present at birth in one child. The other two patients were discovered to have cystic kidneys and hypertension at 3 months of age. Development delay and seizures were ultimately present in two infants; typical cutaneous lesions of tuberous sclerosis developed in only one child. The roentgenographic appearance of the kidneys in the two older children was similar to that of adult-type polycystic kidney disease. Cysts were lined by a distinctive, hyperplastic epithelium in each patient. The diagnosis of tuberous sclerosis may be determined by renal biopsy in infants presenting with cystic kidneys.

Diagnosis, Differential↗
PubMed1975

Nephropathy associated with sickle cell anemia: an autologous immune complex nephritis. I. Studies on nature of glomerular-bound antibody and antigen identification in a patient with sickle cell disease and immune deposit glomerulonephritis.

The nature of the glomerular-bound antibody and the putative antigen was investigated in one of the patients with sickle cell disease and immune deposit membranoproliferative glomerulonephritis by immunohistologic and glomerular antibody elution. Renal proximal tubular epithelial antigen was localized in association with immunoglobulins G (IgG), M (IgM), Clq fraction of the first component of complement (Clq) and the third component of complement (C3) in a granular pattern along the glomerular basement membrane of the patient's kidney. IgG and IgM were eluted from glomeruli. These immunoglobulins fixed to the proximal tubules of normal human kidney by direct immunofluorescence. This localization was abolished by absorption of the eluted immunoglobulins with renal tubular epithelial (RTE) antigen. The IgG eluted from the glomeruli blocked the fixation of rabbit anti-RTE antigen to normal proximal tubular brush border. These studies suggest that the nephritis in this patient was due to deposition of complexes or RTE antigen and specific antibody. An autologous immune complex nephritis may develop in some patients with sickle cell anemia secondary to RTE antigen released possibly after renal ischemia or some other phenomenon causing renal tubular damage.

Adolescent↗