The Pituitary and Prostate: An Endocrine Connection
Taylor P, Perry P, Ibrahim B, Swaminathan K
Correspondence to:
Dr.Krishnan Swaminathan,
Consultant Physician & Endocrinologist,
Ward 14, Victoria Hospital,
Kirkcaldy, Fife
KY2 5AH
Email: krishnan.swaminathan@nhs.net
Fax number: 01592 648049
Abstract:
A 61 year old gentleman presented with polyuria and polydipsia in the absence of diabetes mellitus. This case presentation highlights the diagnostic challenges and surprises in the evaluation of polyuria and polydipsia.
Introduction:
Diabetes Insipidus is a condition characterised by passage of large volumes (> 3 litres/ 24 hours) of dilute urine. The subtypes of diabetes insipidus (cranial, nephrogenic and primary polydipsia) can often pose a difficult diagnostic challenge. It is vital to make the correct diagnosis of these subtypes as it has implications in the management. We report an interesting case of a 61 year old gentleman with polyuria and polydipsia in whom a clinical examination with appropriately directed tests unravelled an unexpected diagnosis.
Case report:
A 61 year old gentleman was referred to the endocrine outpatient clinic with a 4 week history of abrupt onset polyuria (approximately 4 litres/day) and polydipsia. He had no significant past medical history, denied headaches or focal neurological symptoms. His GP had done fasting plasma glucose prior to referral, which was normal at 4.9 mmol/l. The patient had never been on any medications particularly lithium, demeclocycline, antipsychotics or antidepressants. His family history was unremarkable.
On examination, his blood pressure was markedly raised at 200/110mm Hg, cardiovascular, chest and abdominal examination was unremarkable. There were no visual field defects or focal neurology. His renal function was mildly impaired with a raised urea of 10 mmol/l and a creatinine of 189 umol/l, plasma sodium was elevated at 148 mmol/l and the plasma osmolality was 297 mosm/kg. His potassium, liver functions and anterior pituitary hormones were within normal limits.
The initial suspicion was cranial diabetes insipidus in view of the abrupt onset of symptoms and the lack of risk factors for nephrogenic diabetes insipidus (normal levels of calcium, potassium, lack of medication history). The renal impairment was initially thought to be due to hypertensive nephropathy. He went on to have a water deprivation test and this revealed a urine osmolality of between 299-317 mosm/kg throughout the test with urine volumes consistently between 130-150 ml/hr in spite of fluid deprivation. His serum osmolality peaked at 303 mosm/kg during the test. Unfortunately, he could not stay on for the desmopressin challenge at the end of water deprivation. A diagnosis of partial diabetes insipidus was made based on the rise in serum osmolality to >300 mosm/kg, consistently high urine output in spite of the water deprivation and a urine osmolality failing to rise to > 750 mosm/kg. He was started on a trial of desmopressin nasal spray with plans for an outpatient MRI of the pituitary and an ultrasound of kidneys (in view of the renal impairment).
He failed to respond to maximal doses of the desmopressin spray. He was reviewed shortly thereafter in the outpatient clinic and a repeat abdominal examination revealed a vague mass in the lower abdomen. Review of his history did not reveal any obstructive symptoms. An urgent ultrasound of the renal tract was organised the next day and this revealed bilateral hydronephrosis with a post micturition volume of 2 litres with thinning of the right renal cortex (Figs 1& 2). He was admitted under the urologists who diagnosed benign prostatic hypertrophy as the cause of his obstructive uropathy. Bladder catheterization was done followed by a transurethral resection of prostate. This led to a complete cessation of his polyuria and polydipsia. He remains well since his surgery.
Fig 1: Postviod bladder showing urinary retention
Fig 2: Hydronephrosis of the right kidney with thinning of the renal cortex
Discussion:
Medications especially lithium and metabolic disorders are the most common causes of nephrogenic diabetes insipidus1. Paradoxical polyuria and nephrogenic diabetes insipidus due to obstructive nephropathy, though uncommon, has been previously reported 2-4. The pathogenesis is not well understood but thought to be secondary to renal tubular resistance to arginine vasopressin due to increased pressure in the collecting ducts. It is important to think of obstructive uropathy in patients with a documented diagnosis of nephrogenic diabetes insipidus as rapid and full reversibility of symptoms is common after the relief of obstruction, as highlighted in our case.
References:
1. Garofeanu CG, Weir M, Rosas-Arellano MP, Henson G, Garg AX, Clark WF. Cause of reversible nephrogenic diabetes insipidus: a systematic review. Am J Kidney Dis 2005;45(4):626-37.
2. Hong EG, Suh Y, Chung YS, et al. A case of nephrogenic diabetes insipidus caused by obstructive uropathy due to prostate cancer. Yonsei Med J 2000;41(1):150-4.
3. Yoshioka K, Imanishi M, Sakai H, et al. Nephrogenic diabetes insipidus due to hydronephrosis in a patient with a solitary kidney. Clin Exp Nephrol 2003;7(3):243-6.
4. Kato A, Hishida A, Ishibashi R, et al. Nephrogenic diabetes insipidus associated with bilateral ureteral obstruction. Intern Med 1994; 33(4):231-3.