Urinary monitoring excretion

Diuretics, typically spironolactone, form the main therapy, combined with restricted salt intake. Sodium restriction is usually unnecessary where fluid retention is mild, and if marked limitation (less than 40 mmol per day intake) is imposed, may lead to impaired nutrition and is poorly accepted. Diuretic treatment often requires reinforcement with loop diuretics. Treatment can be maintained if urinary sodium excretion is at least 30 mmol per day. Removal of ascites through diuresis requires fluid transfer through the intravascular fluid compartment. If diuresis is too intense the intravascular fluid volume is reduced and hypotension causes hepatorenal failure to follow. The aim should be, through monitoring weight loss, to restrict fluid removal to 0.5 kg per day. In this way the risks of hyponatraemia, renal and hepatic impairment should be reduced. 

Countries affected by iodine deficiency require to develop national programmes to assess the extent and severity of the problem. Once an IDD control programme is initiated monitoring and evaluation are required. There are three major components needed to meet this goal, namely determination of thyroid size and goitre prevalence, the determination of urinary iodine excretion, and the measurement of thyroid function, including serum TSH levels. 

Therapy with hydrochlorothiazide, up to 50 mg twice daily, or chlorthalidone, 50-100 mg daily, is recommended. Loop diuretics such as furosemide and ethacrynic acid should not be used because they increase urinary calcium excretion. The major toxicity of thiazide diuretics, besides hypokalemia, hypomagnesemia, and hyperglycemia, is hypercalcemia. This is seldom more than a biochemical observation unless the patient has a disease such as hyperparathyroidism in which bone turnover is accelerated. Accordingly, one should screen patients for such disorders before starting thiazide therapy and monitor serum and urine calcium when therapy has begun. 

Aspirin has been shown to slightly reduce the natriuretic effect of spironolactone in healthy individuals, possibly by reducing active renal tubular secretion of canrenone, the active metabolite of spironolactone. However, the hypotensive effect of spironolactone and its effect on urinary potassium excretion in hypertensive patients is apparently not affected. Until more clinical data are available on this potential interaction, patients receiving both drugs should be monitored for signs and symptoms of decreased clinical response to spironolactone [65]. 

Beyond avoidance of alcohol, the primary treatment is salt restriction and oral diuretic therapy. Achieving the desired fluid losses in patients with ascites caused by portal hypertension is directly related to sodium balance, not fluid restriction. To monitor these patients, evaluation of urinary sodium excretion, utilizing a 24-hour urine collection, is recommended. However, severe hyponatremia, serum sodium <120 mEq/L, does warrant fluid restriction rapid correction of asymptomatic hyponatremia (patients with cirrhosis usually are not symptomatic until their serum sodium concentrations are <110 mEq/L) is not recommended. 

For those patients with normal to moderately impaired renal function, the cornerstone of initial treatment of hypercalcemia is volume expansion to increase urinary calcium excretion (see Table 49-6). Patients with severe renal insufficiency usually do not tolerate volume expansion they may be initiated on therapy with calcitonin. Patients with symptomatic hypercalcemia are often dehydrated secondary to vomiting and polyuria thus rehydration with saline-containing fluids is necessary to interrupt the stimulus for sodium and calcium reabsorption in the renal mbule. ° Rehydration can be accomplished by the infusion of normal saline at rates of 200 to 300 mL/h, depending on concomitant conditions (primarily cardiovascular and renal) and extent of hypercalcemia. Adequacy of hydration is assessed by measuring fluid intake and output or by central venous pressure monitoring. Loop diuretics such as furosemide (40 to 80 mg IV every 1 to 4 hours) or ethacrynic acid (for patients with sulfa allergies) may also be instiffited to increase urinary calcium excretion and to minimize the development of volume overload from the administration of saline (see Table 49-6). Loop diuretics such as furosemide... 

Adverse effects of oral calcium and vitamin D supplementation include hypercalcemia and hypercalciuria, especially in the hy-poparathyroid patient, in whom the renal calcium-sparing effect of parathyroid hormone is absent. Hypercalciuria may increase the risk of calcium stone formation and nephrolithiasis in susceptible patients. One maneuver to help prevent calcium stones is to maintain the calcinm at a low normal concentration. Monitoring 24-hour urine collections for total calcium concentrations (goal <300 mg/24 h) may also minimize the occurrence of hypercalciuria. The addition of thiazide dinretics for patients at risk for stone formation may result in a reduc-tionof both urinary calcium excretion and vitamin D requirements." ... 

Clinicians should be aware of the factors that result in transcellular potassium shifts. Monitoring 24-hour urinary potassium excretion may be necessary in high-risk patients. 

There are no reports of human nephrotoxicity caused by release of mercury from amalgam fillings. This is supported by experimental data from ten humans where standard measurements of renal function (glomerular filtrate rate, urinary albumin excretion, P2-microglobuUn, N-acetyl-P-D-glucosaminidase) were monitored before and 60 days after the removal of mercury amalgam fillings [102]. 

Treatment is by administration of a chelating agent, penicillamine, to promote urinary copper excretion. Patients are maintained on oral penicillamine for life and require regular monitoring tt> ensure compliance and to check for side effects. Liver transplantation may also be considered, particularly in young patients with severe disease. 

The main feature of pre-eclampsia in pregnancy (pp. 142-143) is hypertension. A rising serum urate concentration is encountered early in the development of pre-eclampsia and is impi>rtant for monitoring the condition, as is the urinary protein excretion and creatinine clearance. 

Glomerular filtration rate should be measured as should urinary protein excretion to monitor her condition. 

If a decoppering agent is used for treatment, the compliance can be tested by repeated measurements of the 24 h urinary copper excretion. This approach is not useful if patients are treated with zinc. The dose of d-penicillamine can be lowered if in a compliant patient urinary copper excretion decreases over time and stabilizes at < 500 p g/day. Efficacy of treatment can be monitored by the determination of free copper in serum, and depending on the presenting symptoms. Liver disease can be assessed by routine liver function tests. Repeated liver biopsies with measurement of hepatic copper content are not helpful. Improvement of neurological symptoms can be documented by clinical examination or by auditory evoked brainstem potentials. In addition, some of the MRI abnormalities are fully reversible on treatment. 

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