Stupor and flaccid paralysis in a patient with end-stage renal failure

(Section Editor: M. G. Zeier)

Eleanora Plotkin1, Eliezer Golan1, Tuvia Shimoni2 and Ze'ev Korzets1

Départments of 1 Nephrology and 2 Emergency Meir Hospital Sapir Medical Center Kfar-Saba and the Sackler School of Medicine University of Tel-Aviv Tel-Aviv Israel

Case

A 77-year-old man was admitted with a 6 h history of a sudden deterioration in mental status. He was known to be suffering from end-stage renal failure (creatinine clearance of 4 ml/min) due to hypertensive nephrosclerosis. He had previously refused dialysis. Relevant past medical history included a right femoro-popliteal bypass, a cerebrovascular accident from which he had fully recovered and hypothyroidism. On examination, he was in a stuporous state with a slurred, unintelligible speech. He had a flaccid quadriparesis, drooping of the left lower eyelid and a flattened left nasolabial fold. His blood pressure was 140/100 mmHg, respiration 20 breaths/min with bilateral basal rales. His biochemistry on presentation is shown in Table 1Go.


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Table 1. Data of patient's biochemistry on presentation compared to normal range

 
The patient's medications prior to admission included furosemide, doxazocin, propranolol, felodipine, minoxidil and L-thyroxine.

Questions

What is the cause of this patient's stupor? What factors contribute to the hypoglycaemia?

Answer to the quiz on preceding page

This end-stage renal failure, non-diabetic patient presented in a stuporous state of 6 h duration. On initial neurological examination, he was thought to have suffered a cerebrovascular accident manifested by a left central facial nerve palsy and right hemiparesis. Laboratory evaluation revealed profound hypoglycaemia. Dextrose infusion resulted in a rapid and dramatic improvement of mental function and complete disappearance of any neurological deficit. Obviously then, the patient's stupor was due to hypoglycaemia. Uraemic hypoglycaemia often presents with neuroglycopenic rather than catecholamine-mediated symptoms.

Renal insufficiency is a very common predisposing condition for hypoglycaemia. In renal failure, hypoglycaemia has usually been associated with insulin therapy, anti-diabetic drug use, or concomitant hepatic or endocrine deficiency. However, spontaneous hypoglycaemia may develop in both diabetic and non-diabetic renal failure patients. Although the precise mechanism for spontaneous uraemic hypoglycaemia is not clear, multiple factors are probably involved in its pathogenesis [1]. Foremost among these is caloric deprivation due to anorexia, vomiting or dietary neglect. Second to the liver, the kidney is the most important site of insulin degradation. Under normal circumstances, the amount of insulin removed and degraded by the kidney approximates 6–8 units in 24 h [2]. Despite the increased peripheral resistance to insulin seen in chronic renal failure, impaired renal clearance of insulin may contribute to spontaneous uraemic hypoglycaemia. However, although elevated insulin levels have been found in some patients, they are for the most part normal. In starvation, renal gluconeogenesis is a major source of glucose. The absence of this supply of glucose in renal failure may also play a role in uraemic hypoglycaemia, as might diminished hepatic glucose production. The latter may result from limited substrate availability, in particular alanine (this being the main amino acid substrate for hepatic gluconeogenesis) [3], enzymatic defects in the gluconeogenetic pathway, or from glycogenolysis. Thus, hepatic and endocrine (adrenal and thyroid) dysfunction serve to aggravate the potential for hypoglycaemia. Finally, the release of counterregulatory hormones, glucagon and catecholamines may be blunted in uraemia due to autonomic neuropathy.

Our patient exhibited many of the factors outlined above. Long-standing uraemia probably led to a chronic malnourished state and associated caloric deprivation. His insulin level was slightly above normal. This was associated with elevated C-peptide levels, thus effectively ruling out an exogenous source of insulin. He was markedly hypothyroid despite being on replacement therapy (either inadequate or non-compliant). ß-blocker administration may have interfered with catecholamine release.

This case serves to highlight the fact that mental deterioration in an end-stage renal failure patient should not offhand be ascribed to uraemic coma or cerebrouas clear accident. Although hypoglycaemia is far less common than glucose intolerance in uraemic patients, it should, nevertheless, be borne in mind.

Notes

Supported by an educational grant from

References

  1. Arem R. Hypoglycemia associated with renal failure. Endocrinol and Metab Clin North Am1989; 18: 103–121
  2. Rubenstein AH, Mako ME, Horwitz DL. Insulin and the kidney. Nephron1975; 15: 306–326[ISI][Medline]
  3. Garber AJ, Bier DM, Cryer PE, Pagliara AS. Hypoglycemia in compensated chronic renal insufficiency: Substrate limitations of gluconeogenesis. Diabetes1974; 23: 982–985[ISI][Medline]




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