Polydipsia defined Polydipsia is defined as increased thirst or greater than normal water consumption. Daily maintenance water requirements for dogs may be calculated from the formula [140 x (body weight in kg.)0.75 ]. Daily maintenance water requirements for cats may be calculated from the formula [80 x (body weight in kg.)0.75]. Normal water consumption usually will not exceed approximately 90 ml/kg/day in dogs, or 45 ml/kg/day in cats. Water consumption of greater than 90 ml/kg/day by dogs or 45 ml/kg/day by cats is evidence of polydipsia.
What volume of urine is normal? Normal urine volume is influenced by several variables. It has been estimated that normal adult dogs in a normal environment will produce approximately 20 to 40 ml of urine per kilogram of body weight per 24 hours (1.0 to 2.0 ml/kg/hour). In one study, normal adult cats produced an average of 28 ml of urine per kilogram of body weight per 24 hours.
Normal 24-hour urine volume for kittens has been estimated to range between 5 and 60 ml per kilogram of body weight. Newborn puppies have a comparatively limited ability to concentrate or dilute urine in response to changes in extracellular fluid volume.
Puppies and kittens are predisposed to rapid dehydration as a result of their higher water requirements, their comparatively greater insensible water losses, and their decreased ability to maximally concentrate urine.
How is polyuria defined? Polyuria is defined as the formation and elimination of large quantities of urine. The term diuresis is also defined as formation of abnormally large volumes of urine. Urine volume in excess of 45 ml/kg/day in dogs, and 40 ml/kg/day in cats is consistent with polyuria. Depending on the body's need to conserve or eliminate water and/or solutes, polyuria may be normal (physiologic or compensatory) or abnormal (pathologic). For example, polyuria is an appropriate response to water consumption in excess of need. However, polyuria is inappropriate when dehydration is present. Without knowledge of additional information obtained from the history, physical examination, results of urinalysis, and so on, the clinical significance of polyuria cannot be reliably determined.
Physiologic polyuria The most common cause of polyuria is physiologic polyuria. It usually occurs as a compensatory response to increased fluid intake.
Verification that a patient has physiologic polyuria may require a provocative water deprivation or vasopressin response test.
Pharmacologic polyuria Pharmacologic polyuria may occur: 1) following ingestion of sufficient quantities of salt to increase thirst, 2) following administration of diuretic agents, 3) following administration of glucocorticoids, especially in dogs, 4) following parenteral administration of fluids, 5) following administration of phenytoin (ADH inhibition), and 6) following administration of synthetic thyroid hormone supplements.
Pathologic polyuria On the basis of different pathophysiologic mechanisms, polyuria may be classified as water diuresis or solute diuresis.
In general, water diuresis is characterized by a urine specific gravity (SG = 1.001 to 1.006 ) and osmolality (Osm = 50 to ± 150 mOsm/kg H2O) below that of glomerular filtrate (SG = 1.008 to 1.012; Osm = approximately 300 mOsm/kg H2O).
Water diuresis commonly results from insufficient antidiuretic hormone (central diabetes insipidus), decreased renal response to adequate concentrations of antidiuretic hormone (renal diabetes insipidus) or excessive water consumption (pathologic thirst including psychogenic polydipsia).
In general, solute diuresis is characterized by a urine specific gravity and osmolality equal to or greater than that of glomerular filtrate. Solute diuresis results from excretion of solute in excess of tubular capacity to absorb it (i.e. glucose in diabetes mellitus), impaired tubular reabsorption of one or more solutes (i.e. urea, creatinine, phosphorus and other solutes in primary renal failure), and/or abnormal reduction in medullary solute concentration that impairs the countercurrent system (i.e. decreased renal medullary urea in patients with portovascular shunts and decreased renal medullary sodium in patients with hypoadrenocorticism).
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.
The specific gravity and osmolality of urine (regardless of volume) formed by patients with acute renal failure will reflect impaired concentrating capacity if a sufficient quantity of nephrons have been damaged (Table 1, p. 8S). The damage may be reversible or irreversible. Irreversible damage may be nonprogressive or progressive.
A state of pathologic oliguria may develop in patients with primary polyuric renal failure if some prerenal abnormality (vomiting, decreased water consumption, cardiac decompensation, etc.) develops (Table 1, p. 8S). The oliguria is related to reduced renal perfusion resulting in reduction in the amount of glomerular filtrate that is formed. If this prerenal cause(s) is reversible and/or if adequate renal perfusion is restored, polyuria will resume.
Oliguria or a nonpolyuric state may develop as a terminal event in patients with chronic progressive generalized renal disease.
Oliguria in the context of reduction of the volume of urine expelled from the urinary bladder during the voiding phase of micturition is associated with diseases of the lower urinary system (ureters, urinary bladder, urethra) that impair flow of urine through the excretory pathway.
Examples of such diseases include: 1) neoplasms, strictures or uroliths that partially occlude the urethral lumen, 2) herniation of the urinary bladder that partially obstructs urine outflow through the urethra or urine inflow through the ureters and 3) rupture of the urinary bladder.
In healthy dogs, very little urine should be retained in the urinary bladder following micturition (approximately 0.1 to 0.2 ml/kg body weight).
What is the definition of anuria? The term anuria has been used to indicate the absence of urine formation by the kidneys, and absence of elimination of urine from the body. It is possible that anuria could occur as a result of complete shutdown of renal function due to lack of renal perfusion caused by thromboembolic disease or severe bilateral renal medullary papillary necrosis. However, anuria is usually associated with total obstruction to urine outflow or rents in the lower urinary tract.