Diagnostic approach to polyuria and polydipsia (Proceedings)


Diagnostic approach to polyuria and polydipsia (Proceedings)

Aug 01, 2008

1. Introduction

A. Polyuria and polydipsia (PU / PD) refer to excessive water consumption and urine production respectively. These are common clinical signs in both dogs and cats.

B. Water consumption exceeding 100 ml/kg or urine production exceeding 50 ml/kg body weight per day is considered abnormal and should be pursued. These numbers have been established in laboratory reared dogs and may not reflect "normal" water consumption in pets. They are to be used only as guidelines.

C. Water consumption can vary greatly from day to day so it is important to have owners subjectively assess water consumption in the home environment for several consecutive days in order to obtain an accurate picture before beginning unnecessary and expensive diagnostic tests. Actual quantification of water consumption can be very difficult and may not be practical for the majority of pet owners.

2. Normal Water Homeostasis

A. Extracellular fluid volume is maintained by regulation of fluid intake and urine production.

B. The thirst center is stimulated by an increase in plasma osmolality (sodium concentration) and/or a decrease in blood volume (hypovolemia) resulting in an increase in water consumption.

C. Increasing plasma osmolality and hypovolemia also stimulate osmoreceptors in the anterior hypothalamus and baroreceptors in the aortic arch resulting in the release of antidiuretic hormone (ADH) from the anterior pituitary.

D. ADH circulates and binds to receptors on the renal tubular cells of the distal tubules and collecting ducts resulting in the production of cAMP. This causes the opening of pores in the luminal membrane of the tubular cells and allows for reabsorption of water from the glomerular filtrate resulting in a concentrated urine. In order for water to be pulled out of the tubule it must move along a concentration gradient maintained by the hypertonic renal medullary interstitium. Loss of this gradient (medullary washout), will result in an inability to concentrate urine even in the face of normal ADH activity. Urea and sodium are argely responsible for maintaining the hypertonicity of the interstitium.

E. The sensation of thirst and secretion of ADH are suppressed when plasma osmolality and blood volume are returned to normal.

3. Differential Diagnosis: Mechanisms of PU/PD

A. Renal disease:

1. Chronic renal failure: A decrease in the number of functional nephrons causes an increase in tubular flow in the remaining nephrons and leads to a solute diuresis. A decrease in urine concentrating ability may be the only laboratory abnormality indicating renal disease (especially in feline patients) presented for PU/PD.

2. Pyelonephritis: Bacterial induced tubular destruction and an increase in renal blood flow cause a decrease in medullary hypertonicity.

3. Primary renal glycosuria (Fanconi's Syndrome): A proximal tubular defect results in renal glycosuria leading to an osmotic diuresis. The blood glucose is normal.

4. Post-Obstructive diuresis: May be seen in previously blocked cats. Due to osmotic diuresis from loss of large amounts of sodium and urea into the urine following relief of urethral obstruction.

B. Diabetes mellitus: Hyperglycemia results in glycosuria and an osmotic diuresis. Threshold for renal glycosuria is a blood glucose of 180 – 220 mg/dl (dog) and 240 – 300 mg/dl (cat).

C. Liver disease: PU/PD may occur as the result of: (1) decreased production of urea which is a major component of the hypertonic medullary interstitium, (2) increased renin and cortisol levels due to a lack of hepatic degradation, (3) increased aldosterone concentration leading to increased sodium concentration, and (4) hypokalemia (see hypokalemic nephropathy).

D. Hyperthyroidism: Increased total renal blood flow reducing the tonicity of the medullary interstitium. Psychogenic polydipsia or primary polydipsia is reported in humans with hyperthyroidism.

E. Hypercalcemia:

(1) Interference with cAMP activation by ADH, (2) damage to ADH receptors, and (3) mineralization of renal tubular cells.

F. Hyperadrenocorticism:

Glucocorticoids interfere with the action of ADH at the renal tubule and decrease ADH secretion by reducing osmoreceptor sensitivity to rising plasma osmolality.

G. Hypoadrenocorticism:

Renal sodium wasting leads to decreased medullary hypertonicity.