Kidney disease, chronic diuretics

Patients with diabetes and hypertension should initially be treated with either P-blockers, ACE inhibitors, ARBs, diuretics, or calcium channel blockers. There is a general consensus that therapy focused on RAAS inhibition by ACE inhibitors or ARBs may be optimal if the patient has additional cardiovascular risk factors such as left ventricular hypertrophy or chronic kidney disease.2,3,59,67... 

In patients with chronic kidney disease and hypertension, ACE inhibitors and ARBs are preferred, usually in combination with a diuretic.67 ACE inhibitors in combination with a thiazide diuretic are also preferred in patients with a history of... 

Potassium-sparing diuretics may cause hyperkalemia, especially in patients with chronic kidney disease or diabetes, and in patients receiving concurrent treatment with an ACE inhibitor, ARB, NSAID, or potassium supplement. Eplerenone has an increased risk for hyperkalemia and is contraindicated in patients with impaired renal function or type 2 diabetes with proteinuria. Spironolactone may cause gynecomastia in up to 10% of patients, but this effect occurs rarely with eplerenone. 

ACE inhibitors decrease aldosterone and can increase serum potassium concentrations. Hyperkalemia occurs primarily in patients with chronic kidney disease or diabetes and in those also taking ARBs, NSAIDs, potassium supplements, or potassium-sparing diuretics. 

Sica DA, Gehr TWB Diuretic use in stage 5 chronic kidney disease and end-stage renal disease. Curr Opin Nephrol Hypertens 2003 12 483. [PMID 12920394]... 

Therapeutic uses Thiazide diuretics decrease blood pressure in both the supine and standing positions postural hypotension is rarely observed, except in elderly, volume-depleted patients. These agents counteract the sodium and water retention observed with other agents used in the treatment of hypertension (for example, hydralazine). Thiazides are therefore useful in combination therapy with a variety of other antihypertensive agents including (3-blockers and ACE inhibitors. Thiazide diuretics are particularly useful in the treatment of black or elderly patients, and in those with chronic renal disease. Thiazide diuretics are not effective in patients with inadequate kidney function (creatinine clearance less than 50 mls/min). Loop diuretics may be required in these patients. 

Secondary gout is a result of hyperuricemia attributable to several identifiable causes. Renal retention of uric acid may occur in acute or chronic kidney disease of any type or as a consequence of administration of drugs diuretics, in particular, are implicated in the latter instance. Organic acidemia caused by increased acetoacetic acid in diabetic ketoacidosis or by lactic acidosis may interfere with tubular secretion of urate. Increased nucleic acid turnover and a consequent increase in catabolism of purines may be encountered in rapid proliferation of tumor cells and in massive destruction of tumor cells on therapy with certain chemotherapeutic agents. 

ACE inhibitors are well tolerated in most patients but are not absent of side effects. ACE inhibitors decrease aldosterone and can increase potassium serum concentrations. Usually the increase in potassium is small, but hyperkalemia is possible. It is seen primarily in patients with chronic kidney disease or diabetes mellitus and in those on concomitant ARBs, nonsteroidal anti-inflammatory drugs, potassium supplements, or potassium-sparing diuretics. Judicious monitoring of potassium and serum creatinine values within 4 weeks of starting or increasing the dose of an ACE inhibitor often can identify these abnormalities before they evolve into more serious complications. 

Diuretics are used widely for the treatment of hypertension see Chapter 32), and loop diuretics appear to lower blood pressure as effectively as Na+-CL symporter inhibitors e.g., thiazides and thiazide-hke diuretics) while causing smaller perturbations in the Upid profile. However, the short elimination half-lives of loop diuretics render them less useful for hypertension than thiazide-type diuretics. The edema of nephrotic syndrome often is refractory to other classes of diuretics, and loop diuretics often are the only drugs capable of reducing the massive edema associated with this disease. Loop diuretics also are employed in the treatment of edema and ascites of hepatic cirrhosis however, care must be taken not to induce encephalopathy or hepatorenal syndrome. In patients with a drug overdose, loop diuretics can be used to induce a forced diuresis to facilitate more rapid renal elimination of the offending drug. Loop diuretics, combined with isotonic saline administration to prevent volume depletion, are used to treat hypercalcemia. Loop diuretics interfere with the kidney s capacity to produce a concentrated urine. Consequently, loop diuretics combined with hypertonic saline are useful for the treatment of hfe-threatening hyponatremia. Loop diuretics also are used to treat edema associated with chronic renal insufficiency. Most patients with ARE receive... 

Drug-drug interactions Lisinoprtl Patients with volume depletion or chronic kidney disease depend on angiotensin to maintain adequate glomerular perfusion. Patients taking lithium are more likely to have transient dehydration, and therefore more likely to have reduced clearance, and more likely to suffer toxicity. Three cases of lithium toxicity after the addition of ACE inhibitors have been reported. In two cases, the ACE inhibitor was added to a diuretic. 

Electrolyte balance Concern about the risk of hyperkalemia associated with ACE inhibitors in patients with chronic kidney disease probably inhibits their use in such patients despite the beneficial effects of ACE inhibitors on progression of chronic kidney disease. In 1094 non-diabetic African-American adults with hypertensive chronic kidney disease, hyperkalemia was associated with increasing age, baseline protein excretion, glomerular filtration rate (GFR), and baseline potassium concentrations. Use of a potassium-wasting diuretic reduced the risk of hyperkalemia [36 ]. 

The most important susceptibility factors are pre-existing chronic kidney disease (CKD eGFR below 60 mVmin) and chronic kidney disease associated with diabetes [15]. Other factors include age over 70 years, the presence of congestive heart failure, nephrotoxic drugs (loop diuretics, metformin, nonsteroidal anti-inflammatory agents), volume depletion, and repeated exposure within short periods of time (under 72 hours). 

In nephrogenic diabetes insipidus the kidney s ability to respond to AVP is impaired by different causes, such as drugs (e.g. lithium), chronic disorders (e.g. sickle cell disease, kidney failure) or inherited genetic disorders (X-linked or autosomal NDI). This type of diabetes insipidus can not be treated by exogenous administration of AVP or AVP analogues. Instead, diuretics (hydrochlorothiazide combined or not with amiloride) and NSAI (indomethacin) are administrated to ameliorate polyuria. 

Documented effects The fruits are used as a diuretic, for swelling due to kidney ailments, to treat kidney stones and are combined with other preparations to treat chronic respiratory disease and as an expectorant. The cedrol fraction, from the essential oil of young branches, together with castor oil is used as a remedy for persistent wounds and ulcers (Minayeva 1991). 

IVaditional use Fresh fruits, infusion of the dried fruits, syrup or jam, or taken with tea, are widely used to quench the thirst, as a tonic, diaphoretic, diuretic, laxative, and sedative, as a remedy to increase the appetite, and to treat chronic gastritis and enterocolitis, stomach and duodenum ulcers, hver diseases, the flu, sore throats, pneumonia, stomatitis, dysentery, typhoid and fever. Water extracts, infusions or tea of the leaves and roots, is commonly used to treat stomach ulcers, chronic gastritis, and kidney stones (Nuraliev 1989). A decoction of the fruits, leaves, and branches is taken to treat cystitis, pyelitis, bronchitis, diabetes, urinary incontinence, eczema, vitiligo, psoriasis, fungal skin diseases, hair loss, and dnring menopanse (Knrochkin 1998). 

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