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Biomedical subjects

E Haapanen

Publications and source records attributed to E Haapanen.

At least 19 recordsLinked to original sources

Acute renal failure following nontraumatic rhabdomyolysis.

The etiology and clinical course of acute nontraumatic rhabdomyolysis and ensuing renal failure was surveyed in a series of 40 consecutive patients. In 28 cases the muscle damage occurred after excessive consumption of ethyl alcohol and/or other intoxications. Prolonged lying immobilized was the reason or contributing factor for rhabdomyolysis in 22 cases. The other evident etiologies were convulsions, vigorous physical exercise, arterial occlusion and hypothermia. Typical local signs of rhabdomyolysis--pain, swelling and weakness of the affected muscles--were absent in one fourth of the patients. In these cases the diagnosis was based on transient elevation of serum creatine kinase enzyme activity. Dialyses were required to manage acute renal failure in 24 subjects. All 36 survivors recovered normal renal function. Neurological defects in the extremities still persisted in 16 patients at three months' follow-up.

Acute Kidney Injury

Guillain-Barré syndrome: quantitative measurement of plasma exchange therapy.

A prospective, controlled study with quantitative measurement of hand muscle-force for plasma exchange treatment in acute Guillain-Barré polyradiculitis was done. Of the 29 patients with severe symptoms, every second patient was selected to the plasma exchange group and all others to the control group. The muscle forces increased and CSF protein decreased significantly more in the plasma exchange group than in the control group, but there were no differences in hospitalization or recovery periods.

Adult

Tienilic acid in patients with impaired renal function.

Diuretic therapy is usually accompanied by biochemical changes, such as hypokalemia, impaired glucose tolerance and hyperuricaemia. Tienilic acid is a new long-acting diuretic with antihypertensive effect, combined with uricosuric property. For the purpose of evaluating the effect of tienilic acid in patients with impaired renal function, eleven patients with hypertension and slight to moderate renal impairment were randomized to either hydrochlorothiazide or tienilic acid therapy. During eight weeks of treatment no changes occurred in serum-creatinine, creatinine-clearance, serum-sodium, or urea. Despite renal impairment, serum uric acid decreased during tienilic acid treatment. Compared with placebo, a significant decrease in uric acid was seen as early as after one week of treatment (p less than 0.01) and after 8 weeks the difference was still of the same order (p less than 0.01). During hydrochlorothiazide therapy, serum uric acid increased progressively. The difference was p less than 0.002 at 4 weeks and p less than 0.0005 at 8 weeks of treatment, compared with placebo. The results of this study show that the uricosuric effect of tienilic acid is maintained in patients with mild to moderate renal impairment.

Adult

Studies on muscle relaxants during haemodialysis.

Signs of neuromuscular block were evident more than 20 hours after the administration of alcuronium to an anuric patient. Complete recovery occurred during haemodialysis. We therefore decided to study the dialysance of three radioactive non-depolarising relaxants during haemodialysis of four patients with chronic renal failure. Although dimethyl tubocurarine and alcuronium were equal as regards dialysance, the concentration of the former, in plasma, falls faster than does alcuronium. It is believed that a larger volume of distribution occurs with dimethyl tubocurarine. In spite of the fact that the dialysance of muscle relaxants is small, haemodialysis might lower the concentration of these substances in the plasma to a level below the critical point which produces paralysis.

Acute Kidney Injury

Hereditary nephronophthisis with a life span of three decades. Light and electron microscopical, immunohistochemical, clinical and family studies.

Familial nephronophthisis was diagnosed in a son and two daughters of a mother who herself died in uraemia at the age of 29 years. The son died at 33 years, two daughters are alive at 30 and 33 years. Our cases suggest a dominant autosomal type of inheritance because the mother married twice; the affected son was from the first marriage and the affected daughters from the second marriage. There was no known consanguinity between the parents. The pathogenesis of the disease can be explained by a slowly progressive process that leads to complete or partial obstruction of the tubules in the corticomedullary area, and also, therefore, to cystic dilatations. Histological evidence for this is provided by the proliferation of fibroblasts around the collecting ducts and other tubules, prominent thickening of the tubular basement membrane, and fibroblasts and collagen fibrils in or inside the thickened basement membranes. An ultrastructural description of affected kidneys is given.

Adult

[Acute anuria].

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Acute Disease