Case series of four patients evaluated for polyuria

Abstract

Central diabetes insipidus (CDI) is characterised by hypotonic polyuria resulting from impaired arginine vasopressin (AVP) secretion by the posterior pituitary. Clinically, CDI must be differentiated from nephrogenic diabetes insipidus (NDI)—renal resistance to AVP's antidiuretic effects—and primary polydipsia (abnormal thirst). NDI is rare in adults except in those treated with lithium; thus, the key challenge is distinguishing CDI from disorders of excessive thirst. While the differential diagnosis is often straightforward, the gold standard water deprivation test (WDT) presents interpretative difficulties. Measuring plasma AVP concentrations enhances diagnostic accuracy, but the required radioimmunoassay is technically demanding and available only in specialised centres. Following a definitive biochemical diagnosis of CDI, further investigation is needed to identify the underlying cause of AVP deficiency. These case examples outline a diagnostic approach to polyuria and revisit the limitations of WDT and desmopressin response testing, particularly in resource-constrained settings. Methodology: Four patients who were referred for additional biochemical testing had their medical records retrieved from the Archives and examined. Every piece of information that could identify patients was anonymised. The bladder was emptied about eight (8 am) in the morning. Due to the lack of an osmometer, blood and urine samples were collected, and the osmolalities of plasma and urine were calculated. Water depletion is uncommon in patients with low-normal or low plasma osmolality, and polyuria is likely the result of an appropriate reaction to a high intake; in contrast, the test was terminated in patients
with high-normal or high plasma osmolality and urine osmolality greater than 750 mmol/kg. Blood and urine are drawn again at 9:00 a.m., and plasma and urine osmolalities are computed hourly for 8 hours. Diabetes insipidus or tubular disease is indicated by the failure of three consecutive urine specimens to be concentrated. The DDAVP test, a powerful synthetic counterpart of vasopressin, was administered to those thought to have diabetes insipidus. Urine and plasma samples were taken an hour following an intramuscular injection of 2 µg DDAVP. Results: Case one (1) WDT was conducted, and plasma osmolality remained within the reference interval while urine osmolality remained hypo-osmolar. Significant elevation of urine osmolality after desmopressin. The diagnosis made was Cranial DI. Case two (2) WDT was conducted, and despite adequate fluid deprivation and subsequent administration of 1-Desamino8-D-Arginine Vasopressin (DDAVP), urine osmolality was persistently low. Findings favour Nephrogenic DI. Case three (3) WDT was conducted, and plasma osmolality increased to the upper limit of the reference interval during the test. Urine osmolality continued to increase but remained < 750 mOsm/kg. Results suggest partial ability to concentrate urine with an increase in plasma osmolality following fluid restriction. Findings were suggestive of Partial DI. Case four (4) WDT was conducted, and plasma osmolality increased above the upper reference limit. Urine osmolality continued to increase but did not exceed 750 mmol/kg. Findings favoured Psychogenic polydipsia. Conclusion: Distinguishing central diabetes insipidus from nephrogenic diabetes insipidus and primary polydipsia requires thorough diagnostic testing, including the water deprivation test and desmopressin response, highlighting the challenges in resource-limited settings and the necessity for accurate biochemical evaluations.