Chronic Pyelonephritis Simulating Adrenocortical Insufficiency

Nussbaum, Harvey E.; Bernhard, W; Mattia, Virginius D.

doi:10.1056/nejm195202212460803

Cited by 26 publications

(3 citation statements)

References 13 publications

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“…It has been reported in glomerulonephritis (Thorn et al, 1944;Sawyer and Solez, 1949;Murphy, Settimi and Kozokoff, 1953), pyelonephritis (Joiner and Thorne, 1952;Enticknap, 1952;Nussbaum, Bernhard and Mattia, 1952), polycystic kidney disease (Borst, 1949), nephrocalcinosis, analgesic nephropathy (Cove-Smith and Knapp, 1973) and renal tract obstruction (Morgan et al, 1978). Although this is apparently a non-specific pathological change, it seems to occur more commonly in tubular than in glomerular disorders (Kleeman, Okun and Heller, 1966).…”

Section: Discussionmentioning

confidence: 99%

Obstructive sodium-losing nephropathy--a case report and review

Nunn

Owens

Scholberg

et al. 1981

Postgraduate Medical Journal

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Summary The third case in the literature of sodium-losing renal disease due to obstruction is presented. The experimental evidence and limited clinical experience is reviewed which suggests that the sodium loss is due to an inappropriate response in the adaptive processes that are initiated by the loss of functioning nephrons. The immediate treatment is by replacement of sodium but in the long term the condition may be reversed by very cautious reduction in sodium intake. Definitive treatment may be indicated where obstruction is the cause and consequently this should be sought in all cases of salt-losing renal disease.

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Section: Discussionmentioning

confidence: 99%

Obstructive sodium-losing nephropathy--a case report and review

Nunn

Owens

Scholberg

et al. 1981

Postgraduate Medical Journal

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“…A tendency to hyperkalaemia was noted by Nussbaum et al (1952), and this was associated with electrocardiographic changes and complaints of paralysis by the patient who died suddenly from what was thought to be hyperkalaemia. Murphy et al (1952) also noticed a tendency for their patient to retain potassium, and were forced to reduce intake in order to avoid dangerous levels in the serum.…”

Section: Discussionmentioning

confidence: 99%

Salt Loss in Chronic Renal Disease

Read¹

1956

BMJ

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It may be that further study of electroencephalographic changes will help to elucidate the nature of the specific changes in cerebral metabolism met in hypopituitarism, and serve as a guide to the tvpe of coma present in difficult cases. SummaryA case of chronic anterior hypopituitarism is described in which two distinct episodes of coma occurred due to differing metabolic disturbances on ea^h occasion. Th2 first episode was associated with hypothermia and hypoglycaemia, and recovery followed direct treatment of these abnormalities successively. On the second occasion coma was due to water-retention, precipitated by a water load, and was again associated with hypoglycaemia. No improvement in clinical state occurred until a diuresis followed the administration of cortisone.Electroencephalography was carried out until reversion to normal rhythm occurred. This reversion was delayed in relation to the clinical state of the patient, but this reversion is further evidence that these changes are secondary to endocrine deficiency rather than to local brain damage.Four metabolic states associated with coma in hypopituitarism are discussed-namely, hypothermia, hypoglycaemia, water-retention, and sodium depletion with dehydration. The danger of water-retention following oral or parenteral fluids is emphasized.

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“…2 patients [5,38] presented with significant hypokalemia, with serum K levels of 2.0 and 3.1 mEq/1, respectively. 1 of the 15 patients [13] whose serum K was never mea sured, had persistent EKG changes characteristic of hy perkalemia.…”

Section: Serum Electrolytes On Admissionmentioning

confidence: 98%