INTRODUDCTION
• Polyuria isurine output of > 3L/day
• It is often accompanied by increased frequency of urination, but the
two conditions are not always associated since the underlying cause is
usually different
3.
Pathophysiology- 1
• Waterhomeostasis is controlled by a complex balance of water
intake, renal perfusion, glomerular filtration and tubular reabsorption
of solutes, and reabsorption of water from the renal collecting ducts.
• When water intake increases, blood volume increases and blood
osmolality decreases, decreasing release of antidiuretic
hormone(ADH) from the hypothalamic-pituitary system. Because ADH
promotes water reabsorption in the renal collecting ducts, decreased
levels of ADH increase urine volume, allowing blood osmolality to
return to normal.
4.
2.
• High amountsof solutes within the renal tubules can also cause a passive
osmotic diuresis (solute diuresis) and thus an increase in urine volume.
The classic example of this process is the glucose-induced osmotic
diuresis in uncontrolled diabetes mellitus, when high urinary glucose
levels (> 250 mg/dL [13.88 mmol/L]) exceed tubular reabsorption
capacity, leading to high glucose levels in the renal tubules; water follows
passively, resulting in glucosuria and increased urine volume.
• Glucose-induced osmotic diuresis in diabetes mellitus is further
increased with use of sodium-glucose cotransporter 2 inhibitors (SGLT2i)
that lower plasma glucose levels by inhibiting renal glucose reabsorption
and increasing renal glucose excretion.
5.
3.
• Therefore, polyuriaresults from any process that involves 1 or more
of the following:
i. Sustained increase in water intake (polydipsia)
ii. Decreased ADH secretion (arginine vasopressin deficiency)
iii. Decreased peripheral ADH sensitivity (arginine vasopressin
resistance)
iv. Solute diuresis
6.
ETIOLOGY
There are severalcauses of polyuria. These can be categorized under
the following major causes.
1. Renal
2. Endocrine
3. Latrogenic
4. Metabolic
5. Psychological
7.
1. RENAL
• NephrogenicDiabetes Insipidus: This occurs when the kidneys are unable to respond to anti-
diuretic hormone (ADH), whose function is to conserve water by reducing urine excretion
resulting in polyuria. The kidney's ability to respond to ADH can be impaired by chronic
disorders including polycystic kidney disease, sickle cell disease, kidney failure, partial blockage
of the ureters, and inherited genetic disorders.
• Fanconi's Syndrome: This syndrome is named after Guido Fanconi, a Swiss pediatrician who first
described the syndrome. Here, the malfunctioning kidney fails to reabsorb certain biomolecules
(glucose, amino acids) and ions (bicarbonate, phosphorus, potassium), thereby causing polyuria.
• Chronic Pyelonephritis: Pyelonephritis is the inflammation of the kidneys due to bacterial
infection. Chronic infections can lead to scarring and impaired kidney function, which can result
in polyuria.
• Chronic Kidney Disease (CKD): This condition causes gradual deterioration of kidney function,
which results in nocturnal polyuria, primarily due to excretion of sodium ions (natriuresis)
causing osmotic diuresis
8.
2. ENDOCRINE
• DiabetesMellitus: Uncontrolled diabetes mellitus can cause polyuria
due to osmotic diuresis.
• Central Diabetes Insipidus: Diabetes insipidus manifests as excessive
excretion of water in the urine. In central diabetes insipidus, polyuria
can occur due to trauma, injury, tumors, and lesions of the brain.
• Cushing's Syndrome: Increased urination is a symptom of Cushing's
syndrome which can arise due to pituitary gland tumor (pituitary
adenoma) and ectopic adrenocorticotropic hormone (ACTH)-secreting
tumor.
9.
3. Lactrogenic
• Diuretics:Polyuria can occur due to recent initiation of diuretics for
excreting excess water in the body e.g. in heart failure or peripheral
edema.
• Alcohol: Drinking too much alcohol can cause polyuria.
• Lithium: A patient having a history of lithium use for treating bipolar
disorder can exhibit polyuria.
• Tetracycline: Polyuria is a potential adverse side-effect of antibiotics
like tetracycline.
10.
4. METABOLIC
• Hypercalcemia:This is the increase in blood levels of calcium. This can
occur due to calcium supplementation during osteoporosis, bone
cancer, or hyperparathyroidism.
• Hypokalemia: In this condition, the blood concentration of potassium
falls. This can occur due to chronic diarrhea, diuretic use, and primary
hyperaldosteronism.
11.
5. PSYCHOLOGICAL
• Polyuriacan occur due to excessive compulsive drinking of water,
technically known as psychogenic polydipsia. This can be due to
anxiety or a history of psychiatric illness.
• Polyuria can occur due to complications of psychotic illness
12.
CLINICAL APPROACH
1. HISTORY
•Onset,
• Duration(abrupt or gradual),
• Volume (measured or estimated)
• Associated symptoms: polydipsia, nocturia, weight loss, fatigue
• Drug history (e.g. diuretics, lithium)Past medical history (DM, CKD,
psychiatric disorders)
13.
2. REVIEW OFSYSTEMS
Should seek symptoms suggesting possible causes, including
• Dry eyes and dry mouth
• Weight loss, and
• Night sweats
14.
PAST MEDICAL HISTORY
•Past medical history should be reviewed for conditions associated
with polyuria, including diabetes mellitus, psychiatric disorders, sickle
cell disease, sarcoidosis, amyloidosis, and hyperparathyroidism.
• A family history of polyuria and excessive water drinking should be
noted. Medication history should note use of any medications
associated with arginine vasopressin resistance and agents that
increase urine output e.g, diuretics, alcohol, caffeinated beverages
15.
PHYSICAL EXAMINATION
• Thegeneral examination should note signs of obesity (as a risk factor for type 2
diabetes mellitus) or undernutrition or cachexia that might reflect an
underlying cancer or an eating disorder plus surreptitious diuretic use.The head
and neck examination should note dry eyes or dry mouth (Sjögren syndrome).
• Skin examination should note the presence of any hyperpigmented or
hypopigmented lesions, ulcers, or subcutaneous nodules that may suggest
sarcoidosis.
• Comprehensive neurologic examination should note any focal deficits that
suggest an underlying neurologic insult and assess mental status for indications
of a thought disorder. Volume status should be assessed. Extremities should be
examined for edema