Approach to Polyuria and Polydipsia

Chapter 15 Approach to Polyuria and Polydipsia



Normal Physiology






Pathophysiology




Mechanisms of Polyuria/Polydipsia







Loss of Renal Medullary Hypertonicity














Differential Diagnosis of Polyuria/Polydipsia




TABLE 15-1 Causes of Polyuria and Polydipsia With Mechanisms and Confirmatory Diagnostic Tests











































































































































































































































































































Disease Mechanism of Polyuria and Polydipsia Confirmatory Tests
Chronic renal disease (S) Osmotic diuresis in remnant nephrons ECC
  Disruption of medullary architecture by structural disease CBC
    Profile
    Urinalysis
    Radiography
    Ultrasonography
Hyperadrenocorticism (W) Defective ADH release and action LDDST, HDDST
  Psychogenic Plasma ACTH
    Ultrasonography
Diabetes mellitus (S) Osmotic diuresis caused by glucosuria Blood glucose
    Urinalysis
Hyperthyroidism (W) Increased medullary blood flow and MSW T4
  Psychogenic Technetium scan
  Hypercalciuria  
Pyometra (W) Escherichia coli endotoxin History
  Immune complex glomerulonephritis Physical
    CBC
    Abdominal radiographs
Postobstructive diuresis (S) Elimination of retained solutes History
  Defective response to ADH Physical examination
  Defective sodium reabsorption Urinalysis
Hypercalcemia (W) Defective ADH action Serum calcium
  Increased medullary blood flow  
  Impaired NaCl transport in loop of Henle  
  Hypercalcemic nephropathy  
  Direct stimulation of thirst center  
Liver disease (W) Decreased urea synthesis with loss of medullary solute Liver enzymes
  Decreased metabolism of endogenous hormones (e.g., cortisol, aldosterone) Serum bile acids
  Psychogenic (hepatic encephalopathy) Liver biopsy
  Hypokalemia Blood ammonia
Pyelonephritis (W) E. coli endotoxin Urinalysis
  Increased renal blood flow Urine culture
  MSW CBC
  Renal parenchymal damage Excretory urography
    Ultrasonography
Hypoadrenocorticism (W) Renal sodium loss with MSW Serum Na and K
    ACTH stimulation
Hypokalemia (W) Defective ADH action Serum K
  Increased medullary blood flow and loss of medullary solute  
Diuretic phase of oliguric ARF (S) Elimination of retained solutes History
  Defective sodium reabsorption CBC
    Profile
    Urinalysis
    Ultrasonography
    Renal biopsy
Partial urinary tract obstruction (S) Redistribution of renal blood flow History
  Defective sodium reabsorption Physical examination
  Renal parenchymal damage  
Drugs (W) Various mechanisms depending on drug History
Salt administration (S) Osmotic diuresis caused by excess sodium administered History
Excessive parenteral fluid administration (W) (polyuria only) Water diuresis caused by excess water administered History
Central diabetes insipidus (CDI) (W) Congenital lack of ADH (rare) Water deprivation test
  Acquired lack of ADH (idiopathic, tumor, trauma) Exogenous ADH test
    ADH assay
Nephrogenic diabetes insipidus (NDI) (W) Congenital lack of renal response to ADH (very rare) Water deprivation test
  Acquired lack of renal response to ADH Exogenous ADH test
    ADH assay
    ECC
Psychogenic polydipsia (PPD) (W) Neurobehavioral disorder (anxiety?) Water deprivation test
  Increased renal blood flow Exogenous ADH test
  MSW Behavioral history
Renal glucosuria (S) Solute diuresis caused by glucosuria Blood glucose
    Urinalysis
Primary hypoparathyroidism (W) Unknown (psychogenic?) Serum calcium
    Serum phosphorus
    Serum PTH
Acromegaly (W, S) Insulin antagonism Neuroradiography
  Glucose intolerance Insulin-like growth factor
  Diabetes mellitus in affected cats  
Polycythemia (W) Unknown (increased blood viscosity?) CBC
Multiple myeloma (W) Unknown (increased blood viscosity?) Serum electrophoresis
Renal MSW (W) Depletion of medullary interstitial solute (urea, sodium, potassium) Gradual water deprivation (3-5 days)
    Hickey-Hare test

ACTH, adrenocorticotropic hormone; ADH, antidiuretic hormone; ARF, acute renal failure; CBC, complete blood count; ECC, endogenous creatinine clearance; HDDST, high dose dexamethasone suppression test; LDDST, low dose dexamethasone suppression test; MSW, medullary washout of solute; PTH, parathyroid hormone; (S), solute diuresis; (W), water diuresis.


Most common causes of polyuria and polydipsia.


Adapted from Bruyette DS, Nelson RW: How to approach the problems of polyuria and polydipsia, Vet Med 81:112-128, 1986.


TABLE 15-2 Differential Diagnoses to Be Considered With Polyuria/Polydipsia




































C Calcium, Cushing, Cancer, Corticosteroids
L Liver insufficiency, Leptospirosis (subacute)
A Adrenal (hyperadrenocorticism and hypoadrenocorticism)
M Metabolic, Mellitus (Diabetes), Malignancy, Medullary washout
P Psychogenic, Pituitary, Polycythemia, Pyometra, Portosystemic shunt, Partial urinary obstruction, Paraneoplastic (hypoglycemia), Postictal
E Endocrine, Electrolytes (increased or decreased calcium, decreased potassium)
D Drugs, Diabetes, Diuresis (post-obstructive, hypertension-induced)
R Renal insufficiency/failure
I Insipidus (nephrogenic, central)
B Brain
S Salty treats, Salty diets


Jul 10, 2016 | Posted by in INTERNAL MEDICINE | Comments Off on Approach to Polyuria and Polydipsia

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