The ins and outs of polyuria and polydipsia - DVM
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The ins and outs of polyuria and polydipsia


DVM360 MAGAZINE


Disorders associated with pathologic polyuria and solute diuresis include chronic primary renal failure, the diuretic phase of acute renal failure, post-obstructive diuresis, diabetes mellitus, hyperadrenocorticism and some hepatic disorders (Table 1).

Polyuria which occurs in association with clinical dehydration (caused by vomiting, diarrhea, etc.) indicates that the kidneys are unable to conserve water in spite of the body's need for water. If renal function were normal, physiologic oliguria would be expected to occur as a compensatory response of the kidneys to restore fluid balance.

Diseases that commonly, but not invariably, are associated with polyuria, vomiting and clinical dehydration include primary renal failure (regardless of cause), diabetic ketoacidosis, some cases of pyometra and some cases with liver disorders. Although polyuria, polydipsia and dehydration may be associated with central diabetes insipidus, nephrogenic diabetes insipidus, hyperadrenocorticism and primary polydipsia, these diseases are not typically associated with severe vomiting.

How is oliguria defined? The term oliguria has been used to describe: 1) decreased urine formation by kidneys, or 2) decreased elimination of urine from the body. Oliguria associated with formation of a reduced quantity of urine is related to renal function, and may be physiologic or pathologic in nature.

Physiologic oliguria Physiologic compensatory oliguria occurs when normal kidneys conserve water in excess of solute in order to maintain or restore normal body fluid balance. Physiologic oliguria is characterized by formation of a small volume of urine of high specific gravity and high osmolality. The production of a decreased volume of highly concentrated urine in patients with prerenal azotemia is a notable example of physiologic compensatory oliguria. Prerenal azotemia is often caused by abnormalities that reduce renal function by reducing renal perfusion with blood (i.e. dehydration, shock, cardiac disease, hypoadrenocorticism). Since blood pressure provides the force necessary for glomerular filtration, marked decrease in blood pressure will result in reduction of glomerular filtrate. A variable degree of retention of substances normally filtered by glomeruli (urea, creatinine, phosphorus, etc.) results.

To combat low perfusion pressure and reduced blood volume, the body secretes ADH to promote conservation of water filtered through glomeruli. Production of urine of high specific gravity, high osmolality, and low volume is the normal response (Table 1, p. 8S). Prerenal azotemia provides evidence that the kidneys are structurally adequate to maintain homeostasis and are initially capable of quantitatively adequate function provided the prerenal cause is rapidly removed. However, if the prerenal cause is allowed to persist, primary ischemic renal disease leading to renal failure may develop.

Pathologic oliguria Pathological oliguria refers to a volume of urine that is inadequate for excretion of the body's normal metabolic wastes. Prompt recognition of pathologic oliguria is important because it dictates the volume of fluid that can safely be administered.

Formation of inappropriately concentrated urine in quantities of less than 0.5 ml/kg/hour is evidence of pathologic oliguria in dogs and cats.

Production of approximately 0.5 to 1.5 ml/hr/kg of urine should be considered inappropriate (i.e. relative oliguria) if it persists in rehydrated patients with acute renal failure. If a patient has adequate renal function, diuresis (>2.0 ml/kg/hour) should occur in association with intravenous administration of fluids to correct dehydration and expand extracellular fluid volume.

Rapid onset of diuresis in an oliguric patient associated with intravenous infusion of fluids suggests that the oliguria had a prerenal component.

Pathologic oliguria may occur during the early phase of acute primary renal failure due to generalized ischemic or nephrotoxic tubular disease (Table 1, p. 8S). The exact pathophysiology involved in the production of oliguria in patients with acute renal failure involves several mechanisms. Depending on the inciting cause(s), any one or combination of the following four pathophysiologic mechanisms may be involved: 1) marked vasoconstriction of preglomerular arterioles, 2) decreased glomerular permeability, 3) obstruction of tubular lumens with casts, or by extraluminal compression associated with edema or inflammation, and/or 4) abnormal reabsorption of filtrate through damaged tubular walls.

Pathological oliguria associated with acute renal failure may persist for hours, days or weeks. However, in some instances its duration is so transient that it is not detected. In this situation, the polyuria may be observed.

In some patients, particularly those with drug-induced nephrotoxicity, the term "nonoliguric" is used to reflect a relatively constant, but still inppropriate, volume of urine that is intermediate between oliguria and polyuria.

Generally, patients with acute nonoliguric renal failure have a more favorable prognosis for recovery than patients with acute oliguric renal failure. However, prognosis is dependent on many factors including specific initiating cause, magnitude and severity of intrinsic damage to renal tissues, and the experience of those providing specific, supportive and symptomatic therapy.


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