Differential Diagnosis Of Polyuria Research Articles

Accidental ketosis-induced polyuria in a toddler: a case report

BackgroundIn the pediatric population, parental concern of recent onset frequent or large volume urination in young children is common.Case presentationA 2-year-old male with no significant past medical history and unremarkable family history was brought to his pediatrician by his mother who reports that the child had been “soaking through his diapers” for the previous two to 3 days. Mother states that patient has not had an appreciable change in the number of wet diapers per day, just the perceived weight/volume of each diaper. The patient’s mother denied any recent illness, apparent abdominal pain, dysuria, or recent changes in his bowel movements. She similarly denied polydipsia, polyphagia, or gross hematuria in the patient. Patient’s diet consists of eating a low carbohydrate with mostly high protein and fat diet that was similar to the paleo-type diet consumed by her and her husband. Meals over the recent days were even lower in carbohydrates than usual as the family was actively trying to consume healthier food options.On physical exam the child was found to be afebrile with a normal physical exam. A urine dipstick was performed and was positive for 2+ ketones and 1+ protein. Urine leukocytes and nitrites were negative, as was urinary glucose. A fingerstick blood glucose sample was 83 mg/dL.Based on the patient’s physical examination, laboratory findings, and the history which revealed a very-low carbohydrate diet, a preliminary diagnosis of ketosis-induced polyuria was made. The patient’s mother was advised to incorporate a greater portion of carbohydrates into her son’s diet, with a follow-up scheduled for the following week. At the follow-up appointment the mother reports that she had continued the patient’s carbohydrate intake and the excessive urine amount per wet diaper has not returned. Repeat urine dipstick confirmed the resolution of the ketonuria and proteinuria.ConclusionThis case illustrates the inadvertent consequences that can occur when parents impose new fad diets on their young children. The recent increase in the popularity of fad diets makes the consideration of alternative diets important to review in the patient history and subsequently include in the differential diagnosis of polyuria.

Osmotic diuresis due to urea as the cause of hypernatraemia in critically ill patients

Hypernatraemia is common in critically ill patients and has been shown to be an independent predictor of mortality. Osmotic urea diuresis can cause hypernatraemia due to significant water losses but is often not diagnosed. Free water clearance (FWC) and electrolyte free water clearance (EFWC) were proposed to quantify renal water handling. We aimed to (i) identify patients with hypernatraemia due to osmotic urea diuresis and (ii) investigate whether FWC and EFWC are helpful in identifying renal loss of free water. In this retrospective study, we screened a registry for patients, who experienced intensive care unit (ICU)-acquired hypernatraemia. Among them, patients with hypernatraemia due to osmotic urea diuresis were detected by a case-by-case review. Total fluid and electrolyte balances together with FWC and EFWC were calculated for days of rising serum sodium and stable serum sodium. We identified seven patients (10% of patients with ICU-acquired hypernatraemia) with osmotic diuresis due to urea. All patients were intubated during development of hypernatraemia and received enteral nutrition. The median highest serum sodium level of 153 mmol (Q1: 151-Q3: 155 mmol/L) was reached after a 5-day period of rise in serum sodium. During this period, FWC was -904 mL/day (Q1: -1574-Q3: -572), indicating renal water retention, while EFWC was 1419 mL/day (Q1: 1052-Q3: 1923), showing renal water loss. While FWC did not differ between time of stable serum sodium and development of hypernatraemia, EFWC was significantly higher during rise in serum sodium. Osmotic urea diuresis is a common cause of hypernatraemia in the ICU. EFWC was useful in the differential diagnosis of polyuria during rising serum sodium levels, while FWC was misleading.

Polyuria and Polydipsia: Diagnostic Approach and Problems Associated with Patient Evaluation

Primary disorders of water balance (central diabetes insipidus [DI], nephrogenic DI, and psychogenic polydipsia) should always be considered in the differential diagnosis of polyuria and polydipsia. In general, animals with these disorders have only one laboratory abnormality: a low urine specific gravity. In most instances, the more common causes of polyuria and polydipsia (e.g., hyperadrenocorticism, chronic renal failure, pyelonephritis, pyometra) have specific and obvious abnormalities associated with the complete blood cell count, the serum chemistry profile, and urinalysis. In some cases, however, a low urine specific gravity may be the only abnormality associated with these more common findings. The workup for polyuria and polydipsia can be tedious, time-consuming, expensive, confusing, and not without significant patient morbidity, especially in those cases with normal or near-normal blood work. This article focuses on the diagnostic approach and problems associated with diagnostic testing in patients with disorders of water balance.

9 Polyuric states in man

This chapter reviews the pathophysiological basis for the mechanisms of polyuria and discusses the causes in detail. A small proportion of patients with CDI are of the idiopathic type, with the majority of causes due to trans-spenoidal surgery, head injury following road traffic accidents, and an autoimmune variant. Indirect methods of investigating polyuria are inaccurate in a significant proportion of cases, and the incorporation of measurements of plasma AVP into a water-deprivation test or hypertonic saline infusion can improve diagnostic accuracy. Non-osmotic tests of AVP secretion are of no value in the differential diagnosis of polyuria. Most patients with CDI can maintain water homeostasis with adequate fluid intake, but desmopressin is a convenient, effective and safe therapy which is recommended on both social and medical grounds. Treatment of NDI remains problematic, as neither thiazide diuretics or indomethacin can completely abolish polyuria, and fluid intake remains of primary importance.

Differential diagnosis of polyuria.

Diabetes insipidus (DI) is a syndrome characterized by chronic polyuria and polydipsia. It can result from any of three basic defects: (a) inadequate urinary concentration caused by a deficiency in the secretion or action of the antidiuretic hormone vasopressin (neurogenic or nephrogenic DI), or excessive intake of water caused by a defect in (b) thirst or (c) psychological function (dipsogenic or psychogenic DI). These four types of DI can be differentiated clinically only if they present in a complete and classical form. However, more sophisticated diagnostic approaches involving assays of plasma vasopressin or closely monitored trials of antidiuretic therapy usually are necessary when the patient has mild or incomplete defects in thirst or vasopressin function. Accurate diagnostic differentiation among the four basic types of DI is essential not only for safe and effective management but also for a proper understanding of the basic physiology and pathophysiology of water homeostasis.

Trials for simplified hypertonic saline test

Hypertonic saline test is indispensable for the evaluation of posterior pituitary function. However the test is not simple, including water loading, urine sampling and at least 45 min of hypertonic saline infusion, mostly because the test relies on urinary osmolality as an index of ADH secretion. The object of this study is try to simplify the test by directly measuring plasma ADH concentration before and after 10 min of hypertonic saline infusion. Intravenous infusion of hypertonic saline (5% NaCl, 0.24 ml/kg/min, for 10 min) was performed on normal subjects, patients with diabetes insipidus and patients with renal failure under chronic hemodialysis. Venous blood samples were obtained seriously including just before and after 10 min of the infusion. ADH was extracted from plasma using Sep-Pak C18 column and assayed by specific RIA. Minimum sensitivity of the assay was 0.25 pg/ml. The hypertonic saline infusion resulted in an increase of plasma osmolality by about 8 mOsm/kg H2O and plasma sodium concentration by 4 mEq/l. Plasma ADH increased from 0.77 +/- 0.09 to 3.42 +/- 0.73 pg/ml (m +/- SE, n = 8, p less than 0.01) in normal subjects of ad lib. water drinking and from 0.55 +/- 0.33 to 2.34 +/- 0.33 (m +/- SE, n = 4, p less than 0.05) in water loaded normal subjects (20 ml/kg of water, 60 min before hypertonic saline infusion).(ABSTRACT TRUNCATED AT 250 WORDS)

Measurement of plasma arginine vasopressin in the differential diagnosis of polyuria

Measurement of plasma arginine vasopressin in the differential diagnosis of polyuria. In children and adolescents (1-18 y, n:65) a linear correlation between plasma arginine vasopressin (AVP) and plasma osmolality (Posm), as well as between AVP and urine osmolality (Uosm) was observed. In polyuric patients AVP was measured following osmotic stimulation. After 12-16 h of water deprivation in control children AVP rose to 7.7±3.2 pg/ml, Posm to 296±9.0 and max. Uosm to 1024±124 mosmol/kg (x±SD, n:12). In patients with various tubular disorders impaired renal concentration was obtained (max. Uosm 370±145, Posm 302±11.6 mosmol/kg, n:7). AVP was higher as compared to the control group (14.0±6.8 pg/ml). In 6 patients with central diabetes insipidus AVP was within the low normal range or below the detection limit of 0.8 pg/ml. By means of an infusion of hypertonic saline solution (5% NaCl, 0.04 ml/kg per min for 2 h) a partial defect in AVP release was separated from a complete one.Whereas in the complete form of central diabetes insipidus also at high Posm (>310 mosmol/kg) AVP was undetectable, it was measurable in the partial form, but inadequately low for concurrent Posm. Measurement of AVP during osmotic stimulation is of significance in the differential diagnosis of polyuria.

A Comparison of Plasma Vasopressin Measurements With a Standard Indirect Test in the Differential Diagnosis of Polyuria

The diagnoses provided by a standard indirect test of vasopressin function were compared with those obtained by radioimmunoassay of plasma vasopressin in 24 patients with nonglucosuric polyuria. All seven cases of severe neurogenic diabetes insipidus diagnosed by the indirect tests were confirmed by the vasopressin assay. However, two of six patients with partial neurogenic diabetes insipidus by indirect criteria had normal vasopressin secretion by the direct assay; one was found to have primary polydipsia, and the other nephrogenic diabetes insipidus. Moreover, three of 10 patients diagnosed as having primary polydipsia by the indirect test had clear evidence of partial vasopressin deficiency by the direct assay. The inability of the indirect test to distinguish accurately between partial neurogenic diabetes insipidus and primary polydipsia may be explained by increased sensitivity to low concentrations of vasopressin in the former disorder and a reduction of maximal concentrating ability in both. We conclude that the incorporation of a vasopressin assay improves accuracy in the differential diagnosis of polyuria.

Diabetes Insipidus Following Cardiorespiratory Arrest

Diabetes insipidus following cardiac arrest and hypoxemic encephalopathy occurred in two patients. In both, severe hypoxemic brain damage was followed within three days by clinical and laboratory features of diabetes insipidus, which were corrected by administration of exogenous vasopressin. Hypothalamic injury resulting in diabetes insipidus should be considered in the differential diagnosis of polyuria and dehydration occurring in critically ill patients who have suffered cardiorespiratory arrest.