Kidneys renal disease

One of the most common cause of hyperkalemia is kidney (renal) disease. Additionally, potassium is released into the blood... 

Tocainide is rapidly and well absorbed from the GI tract and undergoes very fitde hepatic first-pass metabolism. Unlike lidocaine which is - 30% bioavailable, tocainide s availability approaches 100% of the administered dose. Eood delays absorption and decreases plasma levels but does not affect bio availability. Less than 10% of the dmg is bound to plasma proteins. Therapeutic plasma concentrations are 3—9 jig/mL. Toxic plasma levels are >10 fig/mL. Peak plasma concentrations are achieved in 0.5—2 h. About 30—40% of tocainide is metabolized in the fiver by deamination and glucuronidation to inactive metabolites. The metabolism is stereoselective and the steady-state plasma concentration of the (3)-(—) enantiomer is about four times that of the (R)-(+) enantiomer. About 50% of the tocainide dose is efirninated by the kidneys unchanged, and the rest is efirninated as metabolites. The elimination half-life of tocainide is about 15 h, and is prolonged in patients with renal disease (1,2,23). 

Esmolol is iv adrninistered. Maximal P-adrenoceptor blockade occurs in 1 min. Its elimination half-life is about 9 min. EuU recovery from P-adrenoceptor blockade is within 30 min after stopping the infusion. The therapeutic plasma concentrations are 0.4—1.2 lg/mL. It is metabolized by hydrolysis in whole blood by red blood cell esterases resulting in the formation of a primary acid metabohte and free methanol. The metabohte is pharmacologically inactive. The resulting methanol levels are not toxic. Esmolol is 55% bound to plasma protein, the acid metabohte only 10%. Less than 2% of parent dmg and the acid metabohte are excreted by the kidneys. Plasma levels may be elevated and elimination half-hves prolonged in patients with renal disease (41). 

Erythropoietin (Eprex ) is physiologically produced in the kidney and regulates proliferation of committed progenitors of red blood cells. It is used to substitute erythropoietin in severe anemias due to end stage renal disease or treatment of cancer with cytostatic agents. Side effects include hypertension and increased risk of thrombosis. 

Disorders of lipoprotein metabolism involve perturbations which cause elevation of triglycerides and/or cholesterol, reduction of HDL-C, or alteration of properties of lipoproteins, such as their size or composition. These perturbations can be genetic (primary) or occur as a result of other diseases, conditions, or drugs (secondary). Some of the most important secondary disorders include hypothyroidism, diabetes mellitus, renal disease, and alcohol use. Hypothyroidism causes elevated LDL-C levels due primarily to downregulation of the LDL receptor. Insulin-resistance and type 2 diabetes mellitus result in impaired capacity to catabolize chylomicrons and VLDL, as well as excess hepatic triglyceride and VLDL production. Chronic kidney disease, including but not limited to end-stage... 

Renal diseases Mutations in KCNJ1 disiupt the function of Kirl.l in apical renal outer medulla of the kidney. The loss of tubular K+ channel function and impaired K+ flux could prevent apical membrane potassium recycling and lead to antenatal Bartter s syndrome. 

O Chronic kidney disease is a progressive disease that eventually leads to renal failure [end-stage renal disease (ESRD)]. 

The National Kidney Foundation (NKF) developed a classification system for CKD (Table 23-11.1 The staging system defines the stages of CKD based on GFR level, but also accounts for evidence of kidney damage in the absence of changes in GFR, as in stage 1 CKD. The GFR is calculated using the abbreviated Modification of Diet in Renal Disease (MDRD) study equation ... 

FIGURE 23-1. Proposed mechanisms for progression of renal disease. (From Joy MS, Kshirsagar A, Paparello J. Chronic kidney disease Progression-modifying therapies. In DiPiro JT, Talbert RL, Yee GC, et al, (eds.) Pharmacotherapy A Pathophysiologic Approach. 6th ed. New York McGraw-Hill 2005 803, with permission.)... 

Although the kidneys are not considered endocrine glands per se, they are involved in hormone production. Erythropoietin is a peptide hormone that stimulates red blood cell production in bone marrow. Its primary source is the kidneys. Erythropoietin is secreted in response to renal hypoxia. Chronic renal disease may impair the secretion of erythropoietin, leading to development of anemia. The kidneys also produce enzymes. The enzyme renin is part of the renin-angiotensin-aldosterone system. As will be discussed, these substances play an important role in the regulation of plasma volume and therefore blood pressure. Other renal enzymes are needed for the conversion of vitamin D into its active form, 1,25-d i hyd ro xyv itamin D3, which is involved with calcium balance. 

HIV infection1 12 13 CD4+T lymphocyte count Diabetes, heart disease, chronic pulmonary disease, chronic alcoholism Asplenia12 (Including elective splenectomy and terminal complement component deficiencies) Chronic liver disease Kidney failure, end-stage renal disease, receipt of hemodialysis... 

The pathophysiology, clinical manifestations, diagnosis, and treatment of acute renal failure and chronic kidney disease (CKD) or end-stage renal disease are discussed in Chaps. 75 and 76, respectively. 

Each kidney has a large functional reserve such that each organ can, if necessary, do the work of two and individuals with only one kidney can live normally. The diagnosis of renal disease is often delayed because a significant amount of tissue deterioration usually occurs before there are clinical or biochemical signs of dysfunction. 

Adult polycystic kidney disease (APKD) is one of the most common autosomal dominant diseases, affecting about 1/1,000 whites. The key feature of this disease is the progressive accumulation of renal cysts, which ultimately culminate in kidney failure. APKD is responsible for approximately 10% of end-stage renal disease in North America. Patients may also have hypertension, cerebral aneurysms, liver cysts, and cardiac valvular defects. 

As mentioned previously, renal failure markedly reduces total renal clearance, as well as metabolic clearance of nicotine and cotinine (Molander et al. 2000). Reduction of renal clearance is correlated with the severity of kidney failure renal clearance is reduced by half in mild renal failure, and by 94% in severe renal impairment. Markedly elevated levels of serum nicotine have been detected in smoking patients with end-stage renal disease undergoing hemodialysis (Perry et al. 1984). This is explained not only by reduced renal clearance, but also by lower metabolic... 

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