Polyuria hypokalemia

Patients with metabolic alkalosis rarely have symptoms attributable to alkalemia. Rather, complaints are usually related to volume depletion (muscle cramps, positional dizziness, and weakness) or to hypokalemia (muscle weakness, polyuria, and polydipsia). 

The activity of the renin-angiotensin system is reduced with age (Muhlberg and Platt 1999). The ability of the kidney to concentrate urine maximally after water deprivation decreases with age, as does the ability to excrete a water and salt load, particularly during the night. Nocturnal polyuria is common in the elderly (Lubran 1995). Diuretics are commonly used in the elderly. There is an increased risk for hypokalemia and hyponatremia from diuretics in the elderly (Passare et al. 2004). Electrolyte disturbances may also be caused by several types of drugs in the elderly and it is important to monitor serum electrolyte levels in the elderly. Treatment with... 

Paresthesias, hearing dysfunction or tinnitus, fatigue, malaise, loss of appetite, taste alteration, nausea, vomiting, diarrhea, polyuria, drowsiness, confusion, hypokalemia Rare... 

Amiloride Blocks epithelial sodium channels in collecting tubules Reduces Na retention and wasting increases lithium clearance Hypokalemia from other diuretics reduces lithium-induced polyuria Orally active duration 24 h Toxicity Hyperkalemic metabolic acidosis... 

One compound that has been associated with distal tubular injury is amphotericin B, a polyene antifungal agent used in the treatment of systemic mycoses caused by opportunistic fungi. Clinical utility of amphotericin B is limited by its nephrotoxicity, characterized functionally by polyuria resistant to antidiuretic hormone administration, hyposthenuria, hypokalemia, and mild renal tubular acidosis. 

In cases where sufficient tubulointerstitial damage causing impaired concentrating ability has occurred, amiloride is less effective still, it can be used in combination with a thiazide diuretic to reduce polyuria [2]. Moreover, hypokalemia, a common side effect of thiazides, is not observed with amiloride [26]. Amiloride obviates the need for potassium supplementation, which is required when thiazide diuretics are used to treat polyuria and, in addition, is less likely to cause lithium intoxication. Although both lithium and amiloride interfere with distal urinary acidification. 

Patients with secondary hypertension may complain of symptoms suggestive of the underlying disorder, but some are asymptomatic. Patients with pheochromocytoma may have a history of paroxysmal headaches, sweating, tachycardia, and palpitations. Over half these patients suffer from episodes of orthostatic hypotension. In primary aldosteronism, symptoms related to the hypokalemia usually include muscle cramps and muscle weakness. Patients with Cushing s syndrome may complain of weight gain, polyuria, edema, menstrual irregularities, recurrent acne, or muscular weakness and have several classic physical features (e.g., moon face, buffalo hump, hirsutism, and abdominal striae). 

Corticosteroids Hypertension, hyperglycemia, hyperlipidemia, hypokalemia, osteoporosis, avascular necrosis, cataract, weight gain, infections, fluid retention Blood pressure, bone densitometry, glucose, potassium, cholesterol, triglycerides (HDL, LDL) Polyuria, polydipsia, edema, shortness of breath, blood pressure, visual changes, bone pain Urinary dipstick for glucose every 3-6 months, total cholesterol yearly, bone densitometry yearly to assess osteoporosis... 

Carbonic anhydrase inhibitors are used as a long-term treatment for open-angle glaucoma by decreasing intraocular pressure by interfering with the production of aqueous humor. Patients who take carbonic anhydrase inhibitors can experience lethargy, anorexia, drowsiness, paresthesia, depression, polyuria, nausea, vomiting, hypokalemia, and renal calculi. It is because of these adverse side... 

Renal impairment owing to prolonged hypokalemia with dilute urine (inability to concentrate urine), polyuria, nocturia, and polydipsia... 

Most clinical cases of secondary aldosteronism are associated with hypertension or edema. Of course, in hypertension. Starling s law still applies in edema, it does not apply. In either case, persistent hyperaldosteronemia results in sodium retention, which expands the volume of the body fluid by promoting water retention. In hypertension, the expansion concerns mainly the blood volume, and hypertension is aggravated. In edema, the expansion mainly affects the extracellular fluid, and edema is exacerbated. Persistent hyperaldosteronemia in both hypertension and edema leads to hypokalemia with muscle weakness and even paralysis, polyuria, and metabolic alkalosis [33] (see Fig. 9-13). 

In an attempt to compensate for the acidosis, bone salts are mobilized. Unless the patient is treated with alkalies, bone salt mobilization results in osteomalacia. Calcium is excreted in the urine, and the combination of high calcium levels, high pH, and low citrate concentration in the tubular fluid facilitates precipitation of calcium salts, thus leading to nephrocalcinosis. Secondary hyperparathyroidism develops as a consequence of the negative calcium balance. The inability to concentrate urine and the accompanying polyuria result in part from the hypokalemia and in part from the hypercalciuria. 

In nephropathic cystinosis clinical chemistry of blood and urine reveals Fanconi syndrome with glucosuria, generalized hyperaminoaciduria and hyperphosphaturia. Most patients show polyuria and loose potassium and bicarbonate resulting in hypokalemia and renal acidosis. Additional tubular losses of calcium, magnesium and carnitine might also occur. The degree of tubular dysfunction is variable in any patient, but also dependent upon... 

A 39-year-old man with suspected urinary tract infection received amikacin and after 4 days he developed severe renal tubular dysfunction resulting in refractory hypokalemia, hypocalcemia, hypomagnesemia, metabolic alkalosis, and polyuria. This constellation of biochemical abnormalities mimic Type 5 Bart-ter s syndrome (activating mutation of the calcium sensing receptor in the thick ascending loop of Henle and the distal tubule). Laboratory values returned to normal 15 days after discontinuation of amikacin... 

Hydroxysteroid Dehydrogenase DeGciency. Failure to thrive, polyuria, polydipsia, hypertension, hypokalemia, and nephrocalcinosis are the symptoms for apparent mineralocorticoid excess due to lip hydroxysteroid dehydrogenase deficiency (cortisol oxidase deficiency) and/or a steroid ring A reductase defect [31]. In the urinary steroid profile, the excretion of THE is much too low compared with the high THF, 5a-THF and free cortisol excretion [32]. 

---