Urine sodium

Chronic heart failure, cirrhosis, and nephrotic syndrome ° Urine sodium >20 mEq/L... 

All patients with ascites require counseling on dietary sodium restriction. Salt intake should be limited to less than 800 mg sodium (2 g sodium chloride) per day. More stringent restriction may cause faster mobilization of ascitic fluid, but adherence to such strict limits is very difficult. Patients usually respond well to sodium restriction accompanied by diuretic therapy.14,22,31,32 The goal of therapy is to achieve urinary sodium excretion of at least 78 mEq (78 mmol) per day.22 While a 24-hour urine collection provides this information, a spot urine sodium/ potassium ratio greater than 1.0 provides the same information and is much less cumbersome to perform. 

Measure spot urine sodium/potassium ratio to assess adherence to dietary sodium restrictions. 

Assess dietary sodium intake by patient food recall or by spot urine sodium/potassium ratio for appropriate sodium excretion. 

While some clinical and laboratory findings assist in the general diagnosis of ARF, others are used to differentiate between prerenal, intrinsic, and postrenal ARF. For example, patients with prerenal ARF typically demonstrate enhanced sodium reabsorption, which is reflected by a low urine sodium concentration and a low fractional excretion of sodium. Urine is typically more concentrated with prerenal ARF and there is a higher urine osmolality and urine plasma creatinine ratio compared to intrinsic and postrenal ARF. 

Urine sodium Less than 20 Greater than... 

FIGURE 78-1. Diagnostic algorithm for the evaluation of hyponatremia. (CHF, congestive heart failure EABV, effective arterial blood volume SIADH, syndrome of inappropriate antidiuretic hormone UNa, urine sodium concentration Uosm, urine osmolality.)... 

An 87-year-old woman received intra-articular betamethasone (Diprophos) 7 mg on three occasions for painful knee joints over 6 months. Six weeks after the last injection she developed diffuse pain and contractures in the legs, fatigue, nausea, abdominal pain, and weight loss of 6 kg. Both knee joints were tender but there was no effusion. Her serum sodium concentration was 123 mmol/1, serum osmolality 254 mosmol/kg, urine sodium 136 mmol/1, and urinary osmolality 373 mosmol/kg. The syndrome of inappropriate antidiuretic hormone secretion was diagnosed, but despite treatment she remained drowsy and hyponatremic. About a week later, she developed hypotension and symptoms of an acute abdomen. Further investigations showed that her basal cortisol concentration was low (36 nmol/1) but it increased to 481 nmol/1 after a short tetracosactide test, consistent with acute adrenal crisis. She recovered rapidly after treatment with oral hydrocortisone, but still required glucocorticoid substitution several months later. 

A 76-year-old woman taking lisinopril 20 mg/day and metoprolol for hypertension developed headaches, nausea, and a tingling sensation in her arms. Her serum sodium was 109 mmol/1, with a serum osmolality of 225 mosm/kg, urine osmolality of 414 mosm/kg, and urine sodium of 122 mmol/1. She had taken diclofenac 75 mg/day for arthritic pain for 6 years and naproxen for about 1 month. Propoxyphene napsylate and paracetamol had then been substituted and zolpidem had been started. A diagnosis of SIADH was postulated and thyroid and adrenal causes were excluded. Lisinopril was withdrawn and fluid was restricted to 100 ml/day. The serum sodium gradually corrected to 143 mmol/1. 

A woman with a 2-week history of insomnia took zopiclone 7.5 mg nightly and over the next 9 days became confused, lethargic, and depressed, culminating in an overdose of six zopiclone tablets. Her previous medical history included hypertension and two episodes of diuretic-induced SIADH. Her serum sodium was 129 mmol/1 and 4 days later fell to 113 mmol/1. Her serum osmolality was low (240 mmol/kg) and her urine sodium was 20 mmol/1. The serum sodium returned to normal 12 days after withdrawal of zopiclone. 

In the case of the frequently requested sample urine, the term urine —sodium and potassium—is applied. Urine has a different... 

Human urine Sodium benzoate Hydrogen chloride... 

Dietary sodium is absorbed in the GI tract. The sodium balance is regulated by the kidneys. When sodium concentration is low, urine is retained. When sodium concentration is high, then there is increased urine. Sodium ... 

The autonomous, sustained production of AVP in the absence of known stimuli for its release is called SIADH. In this syndrome, plasma AVP concentrations are inappropriately increased relative to a low plasma osmolality and to a normal or increased plasma volume. SIADH may be the result of one of several factors production of vasopressin by a malignancy (such as a small cell carcinoma of the lung), the presence of acute and chronic diseases of the central nervous system, pulmonary disorders, or a side effect of certain drug therapies. In addition, as many as 10% of patients undergoing pituitary surgery have a transient SIADH approximately 8 to 9 days after surgery (when the patient is at home), which responds to water restriction (2 to 3 days) and resolves without recurrence. In SIADH, a primary excess of AVP, coupled with unrestricted fluid intake, promotes increased reabsorption of free water by the kidney. The result is a decreased urine volume and an increased urine sodium concentration and urine osmolality. As a consequence of water retention, these patients become modestly volume expanded. The increase in intravascular volume causes hemodilution accompanied by dilutional hyponatremia and a low plasma osmolality. Volume expan-... 

Smaller vessels may be obstructed with cholesterol emboli, vascular lesions, or platelet plugs, all of which will present as isolated decreased perfusion of the glomeruli. The serum creatinine frequently is increased since the lesions are usually diffuse. However, the urinalysis most commonly will be normal since the kidney itself is not ischemic and the glomeruli are not involved. The urinary indices suggest prerenal azotemia (i.e., a low urine sodium concentration and a low fractional excretion of sodium) in the absence of systemic hypotension or a decrease in effective blood volume. The urine volume may or may not be diminished. However, the onset of oliguria sec-... 

This includes patients with fluid losses caused by diarrhea, excessive sweating, and diuretics. This transient hypernatremic hyperosmolality results in osmotic release of ADH and stimulation of thirst. If sodium and water losses continue, more ADH is released as a result of hypovolemia. Patients who then drink water or who are given hypotonic fluids intravenously retain water and develop hyponatremia. Urine osmolality is generally greater than 450 mOsm/kg, reflecting the presence of ADH and formation of a concentrated urine. The urine sodium concentration is <20 mEq/L when sodium losses are extrarenal, as in patients with diarrhea, and >20 mEq/L in patients with renal sodium losses, as occurs in the setting of diuretic use or adrenal insufflciency. °... 

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