Biochemistry in Chronic Kidney Disease - Essay Example

The Role of Clinical Biochemistry in Chronic Kidney Disease Name Institutional Affiliation Course Date Abstract This paper discusses the role of clinical biochemistry in chronic kidney disease. Chronic kidney disease is irreversible but the onset of symptoms can be slowed down with the appropriate management of the disease. A secondary search was performed to generate the content for this discussion. The inclusion criterion for articles is peer-reviewed and published in credible medical websites such as Pub Med. The background discusses the anatomy of the nephron, the basic and functional unit of the kidney. The understanding gained is that the obstruction of the nephron structures from factors such trauma, infections, inflammation or drugs may compromise the kidney function. Kidney function is compromised when the glomerular and tubular functions are impaired. Filtration by the glomerular and re-absorption and secretion by the tubules are slowed down or impaired leading to toxic metabolites in the blood or important minerals and glucose in the urine. Low glomelar filtration of 30mL/min/1.73m2 or below, serum creatinine, hyperkalemia, and urine protein are some of the common markers of kidney function failure. The article explains the laboratory findings in kidney disease and the causes of the abnormal result. The treatment options which mainly include dialysis and kidney transplant in end stage disease are explained. Introduction The clinical biochemistry in Chronic Kidney Disease (CKD) depends on the state of the nephron, the functional unit of the kidney. Each kidney has millions of nephrons (Tsuboi et al. 2014). Each nephron has a glomerulus and tubules which involve in blood filtration, reabsorption of sediments and secretion of wastes (Scott & Quaggin 2015). Factors that affect these functions usually impair the kidney function leading to the onset of CKD (Grahammer, Wanner, & Huber 2014). This paper provides the details. First, the anatomy of the nephron is explained. Second, the function of the glomerular and tubules in health and disease are explained. Next the paper explains laboratory findings in disease and an explanation of the abnormalities. Finally, the treatment is discusses as well as the follow up and monitoring requirements. a) Anatomy of the nephron with diagrams The nephron is the basic functional unit of the kidney (Tsuboi et al. 2014). The kidney’s physiological function at macroscopic level is because of the combined action of the individual nephrons (Tsuboi et al. 2014). The nephron is a long tube consisting of the glomerulus, proximal convoluted tubule, descending and ascending loop of Henle, distal convoluted tubule, and the collecting duct. The glomerulus is a spherical structure appearing at the nephron’s center as a tuft of glomerular capillaries (Glassock & Rule 2012). It is surrounded by the Bowman’s capsule, a membranous structure which is continuous with the proximal tubule (Scott & Quaggin 2015). Its function is to collect any fluids filtering through the glomerular capillaries and drains it into the proximal tubule. The proximal convoluted tubule is the next section after the glomerulus and it lies within the kidney’s renal cortex. It has permeable cell membranes and reabsorbs the glomerular filtrates including glucose, amino acids, metabolites and electrolytes (Vallon & Thomson 2012). The loop of Henle descends from the proximal tubule and ascends into the renal medulla. Some sections of the loop are thin while others are thick. The glomerular filtrate in the loop has reduced water content and higher sodium concentration (Vallon & Thomson 2012). More water is removed from the filtrate in the loop through osmosis resulting in a more concentrated filtrate. The section joining the ascending loop of Henle away from the glomerulus is the distal convoluted tubule which lies within the renal cortex. Potassium excretion takes place in the distal tubule (Wang et al. 2014). The collecting duct is next and it dips back into the renal medulla and its main function is to collect the final filtrate, which is now urine. The cortical collecting duct, which adjoins the distal tubule, has similar functions to the distal tubule. The medullary collecting duct draws out the urine which is now transported to the renal pyramid (Wang et al. 2014). b) Glomerular and tubular function in health and disease The glomerulus is the filtering system of the nephron while the tubule allows for the filtrate to pass (Scott & Quaggin 2015). Blood enters the glomerulus via the afferent arteriole which branches from the renal artery and subdivides to form a network of capillaries in the glomerulus (Glassock & Rule 2012). These rejoin to form the efferent arteriole by which blood leaves the glomerulus. Urine formation starts in the glomerulus capillaries. Filtration of the blood occurs and the resulting filtrate in the Bowman’s capsule is plasma minus the macromolecular plasma components (Schnaper 2013). The filtrate includes water, ions, glucose, urea, minerals and vitamins (Scott & Quaggin 2015). Larger molecules are restricted from being part of the filtrate by the thin walled capillaries. The force of blood pressure in the large afferent arteriole and the pressure in the Bowman’s capsules pushes the filtrate into the proximal tubule. The tubule is responsible for the re-absorption of the solutes from the filtrate back to the bloodstream (Scott & Quaggin 2015). Substances such as glucose and sodium are reabsorbed until the plasma level reaches the renal threshold. The tubule is also responsible for secretion, a process that involves transportation of solutes into the renal tubule so that they can be excreted in the urine (Scott & Quaggin 2015). Secretion in the tubule allows substances such as hydrogen ions to be eliminated at a faster rate than glomerular filtration. Both re-absorption and secretion are regulated by the selective permeability of the different sections of the renal tubule to water, urea and sodium and the response of the distal collecting tubules to the hormones antidiuretic, aldosterone, and parathyroid (Jimbo & Shimosawa 2014). In health, the kidney manages to dilute to concentrate urine according to the individual’s changing physiological needs and can effectively control electrolyte excretion (Grahammer, Wanner, & Huber 2014). However, in disease, kidney function is impaired which imparts adversarial effects on, blood pressure, blood chemistry, fluid balance, nutrient intake and general state of health (Steinke et al. 2015). The glomerular filtration and renal tubular re-absorption and secretion become negatively affected (Steinke et al. 2015). Glomerular filtration rate (GFR) is the ideal measure of overall kidney function in health and disease (Fraser et al. 2015). The normal GFR varies according to sex, age and body size (Glassock 2013). Normal GFR in young adults is approximately 120 to 130 mL/min per 1.73m2 and the GFR declines with age (Glassock 2013). A GFR level of less than 60mL/min per 1.73m2 shows loss of half or more of the adult level of normal kidney function (Oh, Han & Han 2015). Below this level, the prevalence and complications of chronic kidney disease (CKD) increases (Glassock 2013). c) Laboratory findings with explanation of abnormalities Markers of kidney damage include urine sediment abnormalities, abnormal measurements in blood and urine chemistry, and abnormal findings on imaging studies (Floege et al. 2015). Therefore, blood and urine biochemical tests show the extent of kidney dysfunction. Kidney function tests can be used to screen for the kidney disease and establish its cause and the extent of kidney dysfunction (Tsuboi et al. 2014). Specific tests include GFR level test, blood urea nitrogen test, urine protein test, urine creatinine test, microalbuminuria test, serum albumin test, parathyroid hormone test, complete blood count and glucose, calcium, potassium, phosphorus and electrolyte tests among others (Jimbo & Shimosawa 2014). Serum creatinine levels can reveal abnormality in blood chemistry measurements (Fraser et al. 2015). A finding which shows that the albumin-creatinine ratio is greater than 30 mg/g in spot urine samples is considered an abnormal result (Oh, Han & Han 2015). This abnormality indicates that less albumin is being reabsorbed than creatinine is secreted in the tubules. Urine sediment measures may also reveal the presence of protein in the urine which is an abnormal result. The finding occurs after the kidney is damaged and persistent result is a sign of chronic kidney disease (Oh, Han & Han 2015). Blood urea nitrogen (BUN) should be filtrated from the blood and excreted in the urine. Its presence in the blood is abnormal and usually occurs when the glomerular and tubular functions have slowed down due to disease. Abnormal results may show imbalances in electrolytes, minerals and hormones (Jimbo & Shimosawa 2014) Observations include hyperkalemia, or high potassium levels. The disease disrupts the acid-base balance of the blood. Secretion of phosphorus fails leading to its accumulation in the blood. Tubular re-absorption of hematocrit fails leading to a result showing red blood cell count (Jimbo & Shimosawa 2014). The glomerular filtration rate reveals the kidney dysfunction. A rate of less than 30mL/min per 1.73m2 is a warning that the person should consult with the nephrologist (Wang et al. 2014). Once the level reaches 15mL/min per 1.73m2 the patient should start treatment. Signs of uremia accompany the low GFR (Schnaper 2013). d) Treatment As there is no cure for CKD, the goal of the kidney replacement therapy is to slow the progression of the disease, treat the underlying causes or contributing factors, treat the disease complications and the replace the lost kidney function (Onuigbo, Onuigbo & Musso 2014). The progression of the disease from reversible acute to irreversible chronic disease can be slowed by using therapies that control blood glucose and high blood pressure, and diet (Fraser et al. 2015). Medications on CKD include angiotensin converting enzyme inhibitors (ACE-Is), and angiotensin receptor blockers (ARBs) for treatment of hypertension (Tsuboi et al. 2014). Diuretics can also be administered to prevent edema, potassium levels and blood pressure (Tsuboi et al. 2014). Activated form of vitamin D can be prescribed as the disease progresses to improve bone density and also control secondary hyperparathyroidism (Jimbo & Shimosawa 2014). Phosphate binders can also be prescribed. Erythropoiesis-stimulation agents (ESAs) such as Procrit can also be prescribed to stimulate the bone marrow to produce red cells and minimize the need for blood transfusions (Steinke et al. 2015). At end stage CKD, kidney replacement therapy is used, usually through dialysis or kidney transplantation (Onuigbo, Onuigbo & Musso 2014). Dialysis is usually started after GFR has reached 15mL/min per 1.73m2 (Onuigbo, Onuigbo & Musso 2014). Dialysis is started before the patient becomes very symptomatic or at risk of life threatening complications. Types of dialysis include hemodialysis and peritoneal dialysis depending with how the dialysis is accessed (Onuigbo, Onuigbo & Musso 2014). Successful kidney transplantation can offer the best outcome and quality of life. The challenge is usually in getting a matching donor (Canter 2011). Extensive testing is conducted to identify a match and determine the suitability for transplant (Scott & Quaggin 2015). Transplant recipients require lifelong immunosuppressant medications which may increase the chances of infection and some types of tumors (Canter 2011). e) Follow up confirmatory or monitoring testing if any Careful monitoring of blood levels is required in CKD treatment. The physician usually recommends a schedule or regular follow-up visits. During the visits, the patient’s kidney status and underlying condition will be evaluated (Oh, Han & Han 2015). Regular blood and urine tests are conducted to ensure that the levels are still in the normal or manageable ranges. The follow-up may also consider imaging studies such as ultrasound to rule out obstructions in the renal structure relative to the kidney’s physiological function (Schnaper 2013) Conclusion The role of clinical biochemistry has been discussed in relation to chronic kidney disease. CKD is a progressive disease affecting kidney function. The anatomy of the nephron and functions provides a detailed understanding of the mechanism of the disease. The nephron consists of the glomerular and the renal tubules including proximal and distal tubules. The glomerular is responsible for the filtration of substances from the renal arteriole blood, while the tubules are responsible for secretion and re-absorption of substances to achieve a renal threshold. The persistent presence of excretory wastes such as creatinine in the blood, or important substances such as glucose and hematocrit in the urine is an abnormality that signals failure of kidney function. Blood tests and urinalysis are important tests are important in diagnosing such abnormalities. The reduction in the glomerular filtration rate confirms the onset of kidney failure. Chronic kidney failure is when the condition is irreversible and the patient has to depend on treatments that reinforce the kidney function, replace the kidney function and slow down the progression of the disease. Dialysis and kidney transplants are common treatments. Medications to prevent underlying causes and manage symptoms are provided. Follow-up checkups are mandatory for CKD patients. References: Canter, D, Kutikov, A, Manley, B. 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