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Biomedical subjects

P J Klemmer

Publications and source records attributed to P J Klemmer.

5 recordsLinked to original sources
PubMed2000

Carbon disulfide nephropathy.

A 45-year-old nondiabetic man presented with features resembling diabetic triopathy. He worked in a rayon manufacturing plant and was exposed to toxic levels of carbon disulfide (CS(2)). Clinical abnormalities included peripheral and central nervous system abnormalities as well as retinopathy, dyslipidemia, cardiovascular disease, and nephrotic syndrome. He later developed focal sclerosing glomerulonephritis. The latter has not previously been described in cases of CS(2) exposure. Terminally, he developed end-stage renal disease and progressive dementia, both of which were thought to be consequences of CS(2) exposure earlier in life.

Carbon Disulfide↗
PubMed1978

Saline-induced natriuresis in the dog without prior exposure of the kidney to the physical effects of expansion of the extracellular fluid compartment.

1. Experiments were carried out in dogs in which renal perfusion pressure was reduced 40 min before beginning expansion of the extracellular fluid space by 10% with isotonic sodium chloride solution. Sodium excretion increased up to 590% of control values in spite of the fact that the filtered load of sodium was below that of the control period and circulating mineralocorticoids were not suppressed. 2. The findings indicate that, in the dog, prior exposure of the kidney to the volume-expanded state is not a prerequisite for natriuresis to occur.

Animals↗
PubMed1978

Subacute fluorosis: a consequence of abuse of an organofluoride anesthetic.

A young woman presented with a novel multisystem disease: painful periostitis, osteosclerosis, hypertension, and renal dysfunction. The similarity of some of this clinical picture to fluoride intoxication led to the discovery of massively elevated fluoride levels in serum, urine, and bone. Although initially an enigma, the source of fluoride was later found to be the illicit use of an anesthetic agent, methoxyflurane. This agents is one of a class of organofluorides that, by virtue of biotransformation, is a known cause of inorganic fluoride exposure. Though the drug is potentially nephrotoxic as generally used, exposure to it is transient and has not previously led to discernible bone disease.

Acute Disease↗
PubMedDate not supplied

Electrolyte and water balance in young spontaneously hypertensive rats.

In metabolic balance studies the intake and excretion of sodium, potassium, and water were measured in spontaneously hypertensive rats (SHRs) of the Okamoto-Aoki strain and age-matched Wistar Kyoto rats (WKYs) that were 3 through 13 weeks of age. While fed their usual chow, young SHRs exhibited differences in excretion as compared to WKYs consuming essentially equivalent amounts of food and water. Fractional sodium and water excretion (percent of amount ingested) by SHRs were significantly less during Weeks 4-6 and 6-7, respectively, due to lower rates of urinary excretion. Potassium excretion was less in SHRs at 4-5 weeks. These observations indicate that SHRs retain more urinary sodium, potassium, and water during an early phase of hypertension than normotensive, age-matched WKYs. After 8 weeks of age, fractional excretion of electrolytes and water did not differ appreciably between strains. In another group of rats, sodium intake was restricted and observations were made from 3 through 13 weeks of age. Although SHRs excreted slightly less sodium, cumulative sodium balance was similar weeks of age and reduced the magnitude of the hypertension in 10- through 13-week-old SHRs. At the latter age, arterial pressure was not as high in sodium-restricted SHR as in SHR on the standard sodium diet, but it was elevated above that in either WKY groups. Thus dietary sodium restriction retards the development, but does not prevent the hypertension in SHR.

Animals↗