Pathology and Biochemistry of Chronic Kidney Disease, Including Renal Bone Disease - Essay Example

Pathology and biochemistry of chronic kidney disease, including renal bone disease The kidneys The kidneys are a pair of organs that function to removing metabolic wastes like urea, carbon dioxide, salts, and chemicals from the blood and excreting these wastes as urine. Kidneys also regulate the concentration of body fluids and electrolyte concentrations, arterial pressure, secretion/excretion of hormones and acid-base balance of body fluids (Guyton & Hall, 2005). The main functional filtering unit of the kidney is the nephron. At least 800 thousand nephrons are in one kidney. The initial filtering unit in the nephron is the glomerulus, and the filtrates coming from the glomerulus are formed into urine as it passes the other components in the nephron. Diseases in the kidney cause a significant number of deaths and disabilities worldwide (Coresh, et al., 2007). Acute renal failure is manifested by the kidneys abruptly stopping, although the chance exists that the kidneys could recover, while in chronic kidney disease there is a progressive decline in the function of the nephrons. More specifically, chronic kidney disease is defined as damaged or decreased kidney function measured by a decrease in the glomerular filtration rate (GFR) for a period or three or more months (Levey, et al., 2003). Initial damage to the nephron results in compensatory responses of the remaining nephrons allowing for the continuation of clearance of blood solutes. The compensatory action of the nephrons during early damage is thought to be a major cause of renal damage, because during compensation the glomerular capillary pressure is increased so much that damages are incurred leading to lesions in the glomeruli (Arora & Verelli, 2010). Chronic kidney disease is also caused by hypertension, diabetes, disorders in blood vessels and glomeruli, infections, immune system disorders, congenital disorders, and urinary tract obstructions (Guyton & Hall, 2005). Clinical symptoms for chronic kidney disease are not evident until the number of functional nephrons decreases by 70-75% (Guyton & Hall, 2005). The progressive deterioration in kidney function could ultimately lead to end-stage renal disease where the patient must undergo dialysis to remove wastes from the blood, or transplanted with a new kidney. Chronic kidney disease has 5 stages based on the GFR (National Kidney Foundation, 2002). Patients with the stage 1-3 of the disease do not show symptoms. At stage 4-5 electrolyte balance and endocrine disorders become evident. It is believed that the uremic disorders observed at stage 5 are due to the accumulation of toxins (Arora & Verelli, 2010). Increased retention of potassium (hyperkalemia) occurs due to inability of the kidneys to excrete potassium. Metabolic acidosis results from the inability of the kidneys to produce enough ammonia necessary to react with the endogenous acid and produce ammonium. Phosphates, sulphates, and other organic anions accumulate, causing large anion gaps. Metabolic acidosis increases protein degradation and amino acid oxidation, and reduces albumin synthesis, resulting in protein-energy malnutrition, decreased body mass, and increased muscle weakness. Acidosis also interferes with Vitamin D metabolism and mineral imbalance resulting in renal osteodystrophy or renal bone disease. Renal bone disease can be averted with timely dietary measures and medications like phosphate binders and calcitriol (Renal Resource Center, 2007). Skeletal and extraskeletal complications result from the progression of renal bone disease. In chronic kidney disease, renal bone disease is categorized into four general types: (1) low turnover disease or defective mineralization; (2) high turnover bone disease brought about by high levels of the parathyroid hormone (PTH) levels; (3) beta-2-microglobulin associated bone disease; and (4) mixture of the 3 diseases (Arora & Verelli, 2010). Diagnosis and management of chronic kidney disease Chronic kidney disease is diagnosed by laboratory tests on urine and serum. Serum creatinine as an estimate of glomerular filtration rate, albumin-creatinine ratio in the urine, and examination of urine sediment and dipstick test for erythrocytes and leukocytes are recommended (Levey, et al., 2003). Image analysis by ultrasound can be performed for patients with symptoms of stones, infection, obstruction of the urinary tract and having a family medical history of polycystic kidney disease. Serum electrolytes should be measured on patients who are hypertensive, diabetic, and those who have been exposed to drug toxicity. Other tests include urinary concentration or dilution, and acidification for selected patients who present symptoms of polyuria, metabolic acidosis, metabolic alkalosis, hypo- and hyperkalemia (very high levels of potassium). Kidney function is assessed by analyzing serum creatinine along with a blood urea nitrogen test (Lab Tests Online, 2009). Creatinine clearance is an indication of the efficiency of the kidneys in filtering small molecules out of the blood. A traditional and principal marker of kidney damage is persistent or recurring proteinuria (Kean & Eknoyan, 1999). Proteins are large molecules, and therefore they cannot pass the membranes of the glomeruli into the urine. Glomeruli, being negatively charged, also repel proteins. Size and charge barriers do not allow the passage of proteins into urine, unless the glomeruli are damaged (Proteinuria and microalbuminuria, 2007). Proteins can be measured using reagent strip tests for point of care detection and laboratory tests, including immunoassays (Carter, Tomson, Stevens, & Lamb, 2006). When the protein level is more than 3500 milligrams, extensive glomeruli damage has already occurred. An albumin (or protein)-creatinine ratio higher than 30 mg albumin/g creatinine, is abnormal since the cut-off points are greater than 17 mg/g in males and more than 25 mg/g in females (Warram, Gearin, Laffel, & Krolewski, 1996; (Jacobs, Murtaugh, Steffes, Yu, Roseman, & Goetz, 2002). Glomerular filtration rate (GFR) is currently the best test for detecting kidney disorders. GFR is estimated using a formula that uses serum creatinine value, and gender, age and weight of individual. The GFR has been recommended to be the main criterion in classifying kidney disease. Five stages of chronic kidney diseases have been identified based on the glomerular filtration rate (GFR) (National Kidney Foundation, 2002). Kidney damage has been proposed with normal or increased GFR of > 90 mL/min per 1.73 m2, while kidneys have already failed when the GFR greatly decreased at Read More