Polyuria refers to a urine output of> 3 l / day. It must be differentiated from frequent urination, urinating small amounts at night so the urge at normal or low supply many times a day or more. Both changes can lead to nocturia. Pathophysiology Wasserhomöostase is (even a question of complex regulation) controlled by a complex balance of water uptake, renal perfusion, glomerular filtration and tubular reabsorption of soluble components and reabsorption of water from the renal collecting tubes. If the water consumption increases, the blood volume and increased Blutosmolalität decreases, the release of antidiuretic hormone (also known as arginine vasopressin) from the hypothalamus-pituitary system decreases. Since ADH ADH increase decreased levels promotes water reabsorption in the renal collecting tubes, the urine volume, so that the Blutosmolalität normal. In addition to high levels of soluble constituents within the renal tubules 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 levels of glucose in the urine (> 250 mg / dl), the tubular Reabsorptionskapazität exceed what leads to high glucose levels in the renal tubules. Water follows passively, causing what glucosuria and increased urine volume. Therefore, polyuria resulting by each process that includes: sustained increase of the water absorption (polydipsia) Decreased ADH secretion (central diabetes insipidus) Decreased peripheral ADH sensitivity (diabetes insipidus) Solute diuresis Etiology The most common cause of polyuria in adults is taking diuretics the most common cause of polyuria (see table: causes of polyuria) in adults and children is uncontrolled diabetes mellitus there is no diabetes mellitus are the most common causes of primary polydipsia Central diabetes insipidus Nephrogenic diabetes insipidus U rsachen for polyuria cause suspect results diagnostic approach * water diuresis Central Diabetes Insipidus (partially or completely) Inherited Acquired (due to injury, tumors or other lesions) Abrupt or chronic occurrence of thirst and polyuria sometimes follows trauma, pituitary surgery or hypoxic or ischemic cerebrovascular infarction or occurs during the first weeks of life tests on laboratory test with thirst “ADH-challenge” ADH measurement when diagnosis UNKL ar remains Nephrogenic diabetes insipidus amyloidosis drugs (lithium, cidofovir, foscarnet) hypercalcemia (by cancer, hyperparathyroidism or granulomatosis) genetic disorders sickle cell anemia Sjogren’s syndrome Gradual onset of thirst and polyuria in a patient with prior administration of lithium due to bipolar disorder, with hypercalcemia in associated with hyperparathyroidism or in a child with family members who drink excessive amounts of water with underlying or occurring during the first years of life paraneoplastic disorder. Laboratory tests thirst test “ADH Challenge” polydipsia Primary (hypothalamic lesions in the thirst center of the hypothalamus) psychogenic Anxious middle-aged women Positive history of psychiatric disorders Infiltrated lesions of the hypothalamus (usually sarcoidosis) laboratory tests thirst Test Excessive with “ADH Challenge” hypotonic iv Hydration hospital patients infusions received disappearance to stop the hydration or after the infusion rate has been reduced taking a diuretic Recent introduction of a diuretic because of volume overload ((z. B. for heart failure or peripheral edema) patients who are likely to take secretly diuretics for weight loss z. as a result of eating disorders or concerns about their weight, athletes, young people). Clinical evaluation Adipsic diabetes insipidus polyuria without excessive thirst Sometimes lesions in the hypothalamus region such. B. a germinoma or craniopharyngioma, or recent repair of the anterior communicating artery Sometimes hyperosmolality (z. B. 300-340 mOsm / kg) and hypernatremia without excessive thirst gestational diabetes (resulting from increased metabolism ADH) insipidus (polydipsia with excessive thirst ) and polyuria that develop for the first time during the third trimester (inappropriate normal plasma sodium usually takes about 5 meg / l in late pregnancy ab) with urine osmolality lower than plasma osmolality disappearance 2-3 weeks postpartum Solute diuresis Uncontrolled diabetes mellitus thirst and polyuria with a small child or obese adults with a positive history of type 2 diabetes glucose measurement obtained laboratory tests (e.g. by finger prick method isotonic or hypertonic infusions with saline, hospital patients, the infusions. B. 24-hour urine collection, showing the total Osmolausscheidung [osmolality × volume of urine]) stopping or reducing the supply (polyuria that confirm decisions) Protein gavage All patients tube feeding condition changing gavage at lower protein content (in order to determine whether polyuria improved) eliminating Harntraktobstruktion polyuria after urinary catheterization in a patient with bladder outlet obstruction Clinical evaluation * in most patients s hould the measurement of urine and plasma osmolarity as well be performed by serum sodium. urine osmolality is usually <300 mOsm / kg water diuresis and> 300 mOsm / kg at soluter diuresis. ADH = antidiuretic hormone assessment history In the history of the present illness, the quantities of supplied and excreted fluid should be asked to distinguish between polyuria and frequent urination. In polyuria, patients should according to the age at onset, temporal occurrence (z. B. abruptly or gradually) and all recent clinical factors that may cause polyuria (z. B. infusions, tube feeding, removal of urinary tract obstruction, stroke, head trauma, surgery) are interviewed. Patients should be asked about their level of thirst. In reviewing the organ systems should by symptoms that suggest possible causes are researched; including dry eyes and dry mouth (Sjogren’s syndrome) as well as weight loss and night sweats (cancer). The medical history should discomfort associated with polyuria associated, including diabetes mellitus, mental disorders, sickle cell anemia, sarcoidosis, amyloidosis, and hyperparathyroidism are checked. A family history of polyuria and excessive drinking of water should be considered. considered when drug history the use of all drugs that insipidus associated with diabetes in context, it should (s. Causes of polyuria) and substances that increase urine output, (z. B. diuretics, alcohol, caffeinated beverages) werden.Körperliche investigation in the complete physical examination should be signs of obesity, respected (as a risk factor for type 2 diabetes mellitus) or malnutrition or cachexia, which may reveal an underlying cancer or an eating disorder plus secret use of diuretics. In examination of the head and neck on dry eyes or dry mouth (Sjogren’s syndrome) should be taken. In examination of the skin should hyperpigmented or hypopigmented lesions, ulcers or subcutaneous nodules, suggestive of sarcoidosis, are observed. The comprehensive neurological examination should take into account any focal deficits that may indicate an underlying cerebral infarction and beurteilen.Warnzeichen the mental status for signs of thought disorder, the following findings are of particular importance: Sudden onset or occurrence during the first years of life night sweats, coughing and weight loss, especially when smoked excessively this in the past psychiatric disorder interpretation of the findings the medical history can often be made between polyuria and frequent urge to urinate, but sometimes a sample from 24-hour Sammelurinrin is required. The clinical evaluation may include a reference to the cause of giving (see Table: Causes of polyuria), but tests are usually necessary. Diabetes insipidus is suspected in a history of malignant disease, or chronic granulomatous disease (due to hypercalcemia) or the ingestion of certain drugs (lithium, cidofovir, foscarnet), and rare disorders (sickle cell disease, renal amyloidosis, sarcoidosis, Sjögren’s syndrome), whose manifestations are often striking and polyuria precede. The abrupt onset of polyuria at some point suggests a central diabetes insipidus, as well as the preference of extremely cold or ice water. An occurrence in the first years of life is insipidus usually with inherited central diabetes or diabetes mellitus type 1 or uncontrolled diabetes related. History of diabetes mellitus suggests polyuria caused by congestive heart failure. A psychogenic polydipsia is more common (especially bipolar disorder, schizophrenia or) and not as a first Manifestation.Tests If an excessive urine excretion was confirmed by medical history or measurements in patients with previous psychiatric disorder, a glucose determination should be carried out by means of serum or finger test to a exclude uncontrolled diabetes. If it’s not a hyperglycemia, tests are required: Serum and urine chemistry (electrolytes, Ca) serum and urine osmolality and sometimes plasma ADH levels These tests will be on hypercalcemia, hypokalemia (due to secret Diuretikaeinnnahme) and hypernatremia or hyponatremia tested. Hypernatremia (Na> 142 mmol / l) indicates excessive free water loss due to diabetes or central diabetes insipidus out. Hyponatremia (Na <137 mmol / l) is indicative of excessive free water absorption as a result of polydipsia. Urine osmolality is usually <300 mOsm / kg water diuresis and> 300 mOsm / kg at soluter diuresis. If the diagnosis remains unclear, measurements of serum and sodium concentration in the urine and the osmolality should be conducted in response to a thirst testing and administration of exogenous ADH. Because a severe dehydration sequence can be of this test, this should only be performed while patients are under constant supervision. Typically, a hospital stay is required. In addition, patients with suspected on a psychogenic polydipsia is to be monitored to prevent secret drinking. Various protocols can be used in water removal tests. Each protocol has some limitations. Typically, the test will begin in the morning with the determination of the patient’s weight, taking a blood sample for measurement of serum electrolyte concentrations and osmolality and with the determination of urine osmolality. Spontaneous urine is collected every hour to determine the specific gravity and the osmolality measured. The removal of water is continued until orthostatic hypotension and tachycardia postural occur has the body weight is reduced by ? 5%, or the urine concentration is increased not more than> 30 mOsm / kg in successively removed spot urine samples. Values ??for serum electrolytes and osmolality are measured again, and 5 units of an aqueous solution are vasopressin s.c. injected. 60 minutes after injection, a final urine sample for the determination of osmolality is removed and ended the test with it. A normal reaction would be a maximum increase in urine osmolality after dehydration (> 700 mOsm / kg), and after injection of vasopressin osmolality does not increase by more than an additional 5% interest. In central diabetes insipidus patients are not usually able to concentrate the urine on the plasma osmolality out, but can after administration of vasopressin their urine osmolality increase (central diabetes insipidus). The increase in urine osmolality is insipidus 50-100% with central diabetes insipidus compared to 15-45% with partial central diabetes. In patients with nephrogenic diabetes insipidus patients can not focus on the plasma osmolality addition, the urine and point to the administration of vasopressin no reaction (nephrogenic diabetes insipidus). Occasionally, the increase in urine osmolality insipidus be up to 45% in case of partial diabetes, but overall these figures are much lower than those (<300 mOsm / kg in the control) occur at partial central diabetes insipidus. In psychogenic polydipsia, the urine osmolality is <100 mOsm / kg. A gradually declining water intake leads to decreasing urine output, increased plasma and urine osmolality and serum sodium concentration. Measurement of circulating ADH is the most direct method for the diagnosis of central diabetes insipidus. The concentrations are at the end of thirst assays low and correspondingly increased insipidus (prior to injection with vasopressin) with central diabetes insipidus in diabetes. However, ADH levels are not routinely available. In addition, the thirst attempt to deliver accurate results so that a direct ADH-determination is rarely necessary. When measured, ADH values ??should be checked at the beginning of the water removal tests, if the patient is well-hydrated; ADH levels should decrease during intravascular volume increases. Therapy Treatment varies depending on the causes. Conclusion use of diuretics and uncontrolled diabetes are common causes of polyuria. Are no diabetes and no use of diuretics diagnosed, the most common causes of chronic polyuria primary polydipsia and central diabetes insipidus and nephrogenic diabetes insipidus. Hypernatremia usually points to central or nephrogenic diabetes insipidus out. Hyponatremia is characteristically at polydipsia. Sudden onset of polyuria indicates central diabetes insipidus out. A thirst test may help in the diagnosis, but should only be made if the patient is closely monitored.