Pharmacology; Clinical review assignment: Renal failure Essay

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Pharmacology; Clinical review assignment: Renal failure

Renal failure is an increasing concern in Australia, with over 54 people dying every day from kidney related disease. The incidence of this pathology has been shown to be growing, with the number of people on dialysis rising by 4% from 2010 to 2011 (National Kidney Foundation, 2013). It is estimated that approximately 1.7 million Australians over the age of 25 show signs of renal failure, either chronic or acute. Indigenous Australians are also four times more likely to die from renal failure than non-indigenous Australians (Australian Bureau of Statistics, 2006). Signs of renal failure often show themselves in the form of reduced kidney function, proteinuria (protein in the urine) or haematuria (blood in the urine).

Renal failure is a condition involving the failure of the kidneys, or more precisely the nephrons within the kidneys. The nephron is the functional unit of the kidney, with approximately 1.5 million working to filter blood of wastes and reabsorb water and electrolytes necessary to maintain homeostasis (U.S. Patent No. 5,092,886A, 1992). Renal failure occurs when the kidneys fail to filter blood adequately, it is often undetected until late stage failure has occurred. There are two main forms of renal failure; acute kidney disease and chronic kidney disease, both with underlying pathologies (U.S. National Library of Medicine, 2013).

Treatment for renal failure involves either dialysis; filtering of the blood to remove metabolic wastes, or a kidney transplant, which is not a cure and requires permanent care and maintenance post-surgery. As of December 2012, 1080 people are waiting for a kidney transplant in Australia (Better Health Channel, 2013). It is important for paramedics to recognise and understand the underlying pathology behind renal failure as the condition results in a wide range of secondary effects & has many different presentations, with some as simple as headaches and “stomach pain”; pain in the kidney region, and more serious presentations such as metabolic acidosis (National Kidney Foundation, 2013).


All 1.5 million nephrons in the kidney are working constantly to filter blood. The kidneys receive approximately 25% of cardiac output via the afferent arteriole, into the bowman’s capsule which surrounds the glomerulus. The glomerulus is often described as a colander, as it is semi-permeable, only allowing certain things to pass through it. The kidneys main functions are to filter the blood, but they also have many other functions, such as regulating acid/base and fluid/electrolyte balances, reabsorbing water and electrolytes and excreting urine. “In addition, the kidneys excrete metabolic waste products, including urea, creatinine, and uric acid, as well as foreign chemicals” (DeRossi & Cohen, 2008).

The kidneys also serve an endocrinological function, “secreting rennin, the active form of vitamin D, and erythropoietin. These hormones are important in maintaining blood pressure, calcium metabolism, and the synthesis of erythrocytes, respectively.” (DeRossi & Cohen, 2008). The progression of renal failure is often undetected, with renal function able to continue until 50% of the nephrons per kidney are destroyed. After nephrons are destroyed they never regenerate (Tilgner, n.d.). Compensatory buffer mechanisms exist in the body to counterbalance the effects of renal disease. As the kidneys are responsible for water and electrolyte balance, shifts in solute concentrations due to nephron destruction can be seen. Isosthenuria, which is excretion of urine that has not been concentrated by the kidneys and therefore has the same osmolality/gravity as plasma, is the first clinical sign of impaired renal function.

Water along with sodium is flushed from the body resulting in dehydration & an electrolyte imbalance (DeRossi & Cohen, 2008). “In a healthy body, the acid-base balance is maintained via buffers, breathing, and the amounts of acid or alkaline wastes in the urine; this is because the daily load of endogenous acid is excreted into the urine with buffering compunds such as phosphates.” (DeRossi & Cohen, 2008). When the kidneys functions are impaired, a backlog of hydrogen (H+) ion occurs and the nephrons ability to excrete acid becomes inadequate. This results in ketoacidosis, a condition in which the body’s pH falls dangerously below it’s normal homeostatic range, commonly detected by the ‘fruity’ scent of a patients breath which occurs due to acetone; “a direct byproduct of the spontaneous decomposition of acetoacetic acid” (DiTomasso, Golden & Morris, 2010).

Diagnostic tools;

The main ways of diagnosing renal failure include serum chemistry/blood tests, urinalysis and creatinine clearance tests. Serum chemistry is the analysis of blood, when diagnosing renal failure, changes in “Sodium, chloride, blood urea nitrogen (BUN), glucose, creatinine, carbon dioxide, potassium, phosphate, and calcium levels provide a useful tool to evaluate the degree of renal impairment and disease progression.” (DeRossi & Cohen, 2008). The most important of these are creatinine and blood urea nitrogen, both of which are byproducts of protein metabolism which in healthy people is excreted in urine after filtration. In patients with renal failure the levels of createnine and BUN increase to toxic levels, indicating significant functional loss of the kidneys (“Creatinine Levels and BUN,” 2012).

Urinalysis involves examining a patients urine sample, detecting protein, blood, determining osmolality and microscopic examination (Klatt & Georgia, 2013). The main indications of renal failure that urinalysis detects are hematuria and protienuria. Hematuria is defined as “…the presence of red blood cells in the urine. It can be characterised as either “gross” (visible to the naked eye) or “microscopic” (visible only under the microscope)” (“Blood in the urine (Hematuria)”, 2013). Hematuria is commonly benign in younger age groups, with cases of patients less than 40 years old almost always benign. In older age groups hematuria is seen as more serious, prompting medical investigation into the pathology to rule out other causes, such as infection or cancer, as many different types of cancers (bladder, kidney, prostate, urethral) also present with hematuria (American Urological Association, 2005).

Proteinuria is another indication of renal failure, occurring when urine samples contain an elevated level of protein, or albumin, which is the main protein in the blood (National Institute of Health, 2010). Proteins are large molecules and should not pass through golmerular filtration. “The upper limit of normal urinary protein is 150 mg per day; patients who excrete > 3g of protein per day carry a diagnosis of nephrotic syndrome“ (DeRossi & Cohen, 2008). A creatinine clearance test is another diagnostic tool used to determine renal failure, focusing on the glomerular filtration rate to determine the level of functioning renal nephrons. Creatinine is a metabolic by-product of creatine, which remains at a constant value in the urine.

It is caused by breakdown of muscle tissue, and is 100% filtered by the glomerulus. No reabsorption of creatinine should occur in normal functioning tubules within the nephron (National Institute of Health, 2010). This diagnostic test is done via collecting a urine and blood sample within 24 hours. “In chronic renal failure and in some forms of acute disease, the GFR is decreased below the normal range of 100 to 150 mL/min. Advancing age also diminishes the GFR, by approximately 1 mL/min every year after age 30 years.” (DeRossi & Cohen, 2008).

Acute vs. Chronic;

Renal failure classification is broken down into two different parts; onset and location. Renal failure can be acute; occurring within a timeframe of days to weeks, or chronic; renal failure that develops slowly over years. The location of the failure is the second criteria, determining the type of destruction within the nephron (pre-renal, renal, intrinsic or post-renal) (The Renal Association, 2012). Determining the type of renal failure is important as acute renal failure is mostly curable, whereas chronic renal failure is progressive and irreversible, often leading to death. Acute renal failure is characterised by the rapid loss of kidney function, occurring over a few days to weeks, causing azotemia, a condition where a build-up of nitrogenous wastes products occurs, causing metabolic acidosis (DeRossi & Cohen, 2008).

It can be broken down into sections based on where the failure is occurring within the nephron. Pre-renal failure occurs due to a reduction in blood flow/renal perfusion to the kidneys, causing loss of function. The kidney remains undamaged in this condition, with the problem being based solely on blood flow. It is the most common type of acute renal failure and can occur as a secondary illness from “almost any disease, condition or medicine that causes a decrease in the normal amount of blood and fluid in the body” (WebMD, 2013). Post-renal failure is less common, and is caused by an obstruction of the flow of urine “from the kidneys at any level of the urinary tract and that subsequently decreases the GFR” (WebMD, 2013). It is most commonly caused by prostatic enlargement or cervical cancer, usually found in older males. Intrinsic renal failure is the final type of acute renal failure, occurring from direct damage/trauma to the kidneys.

The most common types of intrinsic renal failure are “acute tubular necrosis (ATN), acute glomerulonephritis (AGN) and acute interstitial nephritis (AIN)” (WebMD, 2013). Causes of the decreased blood-flow/obstruction include; surgery, cardiovascular disease, direct trauma/impact to the kidneys, severe burns, severe muscle injury or severe physical exertion (WebMD, 2013). Chronic renal failure focuses around nephron destruction. Renal conditions such as glomerulonephritis affects the filtration rate of the glomerulus, while polycystic kidney disease involves the failure of the renal tubules. Nephrosclerosis interferes with blood perfusion, but the most common diagnosis of chronic renal failure is “diabetes mellitus, followed by hypertension, glomerulonephritis and others” (DeRossi & Cohen, 2008). Although causes vary, each condition shares the common trend of irreversible nephron destruction.

Application to paramedic practice:

Paramedics must be considerate of all patients with renal impairments. Prophylactic measures are often taken in renal patients, managing “diet, fluid, electrolytes and calcium-phosphate balance”, as well as dietary modifications to counterbalance the common difficulties renal patients have with hypertension, oedema and weight gain (DeRossi & Cohen, 2008). Emergency care workers should be weary to maintain a blood pressure lower than 130/85mmHg. Bleeding disorders and anaemia are common conditions patients with renal failure will suffer from. Haemorrhaging and bruising are common. “The antidiuretic hormone vasopressin has been shown to be effective int he short term management of bleeding in patients with renal failure” (DeRossi & Cohen, 2008).

Renal patients on dialysis should not have their intravenous injection site compromised by any medication an ALS paramedic may administer. Blood flow through the arm must not be blocked or obstructed, and as these patients are immunocompromised, efforts to avoid sources of infection must be made (DeRossi & Cohen, 2008). Pharmacotherapeutics is a serious concern for anyone treating a renal patient, as most drugs are excreted by kidney, “and renal function affects drug bioavailability, the volume of drug distribution, drug metabolism and the rate of drug elimination.” (DeRossi & Cohen, 2008).

Drug dosage schedules must be altered according to the amount of residual renal function. Drugs that would normally be safe for most patients may be toxic in patients with renal failure. “The plasma half-lives of medications that are normally eliminated in the urine are often prolonged in renal failure and are effectively reduced by dialysis. Even drugs that are metabolized by the liver can lead to increased toxicity because the diseased kidneys fail to excrete them effectively. Theoretically, a 50% decrease in creatinine clearance corresponds to a twofold increase in the elimination half-life of any medication excreted fully by the kidneys.” (DeRossi & Cohen, 2008)

Knowledge on the pharmacology on all ALS paramedic drugs must be known as certain drugs are nephrotoxic and should not be administered. The early recognition of signs of renal failure is important as mortality rates from acute renal failure (the most common type of renal failure) are high, remaining constant over the past 40 years at approximately 40-70% (Fry & Farrington, 2006).


National Kidney Foundation. (2013). Facts on CKD in Australia. Retrieved from

Australian Bureau of Statistics. (2008). National Aboriginal and Torres Strait Islander Health Survery Retrieved from

Dobos-Hardy, M. (1992). U.S Patent No. 5,092,886A. Boston, Massachusetts. Patent Buddy.

U.S. National Library of Medicine. (2013). Kidney Failure. Retrieved from: Better Health Channel. (2013). Kidney Failure. Retrieved from: National Kidney Foundation. (2013). What are the risk factors for kidney disease? Retrieved from DeRossi, S. & Cohen, D. (2008). Renal disease. Burket’s oral medicine, 11(2), 407- 427. Tilgner, S. (n.d.). Urinary – Kidney support. Journal for the Clinical Practitioner, 10(3), 1-13. DiTomasso, A., Golden, A. & Morri s, J. (2010). Handbook of Cognitive-Behavioural
Approaches in Primary Care. New York, NY: Springer Publishing Company. DOI: 10.1037/O.0027784 Creatinine Levels and BUN. (2012). Retrieved from Blood in the urine (Hematuria). 2013. Retrieved from: Klatt, E., Georgia, S. (2013). Urinalysis. Retrieved from: WebMD. (2013). Prerenal Acute Renal Failure. Retrieved from: American Urological Association. (2005) Hematuria. Retrieved from National Institute of Health. (2010). Proteinuria. Retrieved from National Institute of Health. (2010). Creatinine Clearance. Retrieved from The Renal Association. (2012). Acute Kidney Injury. Retrieved from Fry, A., Farrington, K. (2006). Management of acute renal failure. Postgraduate Medical Journal, 82(964), 106-116.

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