Renal insufficiency drug absorption

Oral bisphosphonates are poorly absorbed (less than 5%). Taking them in the presence of food or calcium supplementation further reduces absorption. After absorption, bisphosphonate uptake to the primary site of action is rapid and sustained. Once attached to bone tissue, bisphosphonates are released very slowly. These drugs are not metabolized and are excreted renally. They are not recommended for use in patients with renal insufficiency. 

Altered renal filtration, secretion, and/or absorption can have dramatic effects on the pharmacokinetics of a drug. The impact depends on the fraction of drug normally eliminated unchanged by the kidney and on the degree of renal insufficiency. 

The highly polar ionic character of EDTA limits its oral absorption. Moreover, oral administration may increase lead absorption from the gut. Consequently, EDTA should be administered by intravenous infusion. In patients with normal renal function, EDTA is rapidly excreted by glomerular filtration, with 50% of an injected dose appearing in the urine within 1 hour. EDTA mobilizes lead from soft tissues, causing a marked increase in urinary lead excretion and a corresponding decline in blood lead concentration. In patients with renal insufficiency, excretion of the drug—and its metal-mobilizing effects—may be delayed. 

However, resistance to loop diuretics can occur by various mechanisms (36). These include poor adherence to therapy, poor absorption, progressive worsening of heart failure, excess volume loss, renal insufficiency, secondary hyperaldosteronism, and hypertrophy of the tubular cells of the distal nephron. Resistance due to inadequate drug absorption—either its speed or extent—is common with furosemide, which is poorly absorbed (34). Once recognized, this hurdle to response can be overcome by using loop diuretics that are predictably well absorbed, such as bumetanide and torasemide or by giving intravenous furosemide (37). 

The aminoglycosides are highly polar and, thus, poorly absorbed from the gastrointestinal (GI) tract. Instillation of these drugs into body cavities with serosal surfaces may result in rapid absorption and unexpected toxicity (e.g., neuromuscular blockade). Toxic levels also may result from sustained topical application to large wounds, bums, or cutaneous ulcers, particularly with renal insufficiency. Long-term oral or rectal administration of aminoglycosides may result in accumulation to toxic concentrations in patients with renal impairment. 

The Pharmacokinetics section of each chapter covers absorption, tissue distribution, elimination, and body fluid concentrations. Such pharmacokinetic information is usually not included in other sources and may be useful in forensic investigations or in the clinical setting regarding use of the product in patients with renal or hepatic insufficiency. A section on Adverse Effects and Toxicity follows and includes detailed information on case reports of adverse reactions to the herb. The Interactions section includes discussions of interactions between the supplement and drugs or foods. The Reproduction section follows and is generally limited because of lack of information. Each chapter ends with a discussion of Regulatory Status of the product. The amount of information included in each of these sections varies according to availability. 

Hypomagnesemia is usually associated with disorders of the intestinal tract or kidney. Drugs or conditions that interfere with intestinal absorption or increase renal excretion of magnesium can result in hypomagnesemia (Table 50-6). Decreased intestinal absorption as a result of small bowel disease is the most common cause of hypomagnesemia worldwide. These disorders include regional enteritis radiation enteritis ulcerative colitis acute and chronic diarrhea pancreatic insufficiency and other malabsorptive syndromes small-bowel bypass surgery and chronic laxative abuse. ... 

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