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Kidney care and renal disease.

The kidneys are essential in the maintenance of homeostasis. Renal dysfunction causes multiple, complex effects throughout the body. Kidney function can be impaired acutely, following infection or trauma, or it may develop slowly as a complication of chronic diseases such as diabetes or hypertension. The number of people in New Zealand requiring treatment for renal disease is increasing and incidence is disproportionately high in Maori and Pacific populations, but this is not solely due to their higher incidence of diabetes and hypertension. An appreciation of the roles of the kidney promotes better understanding of the consequences of renal dysfunction. Recognising, and being vigilant for, the complex pathophysiological processes in acute and chronic renal impairment enhances best care for patients.

[FIGURE 1 OMITTED]

INTRODUCTION

Renal disease is expected to place an increasing burden on the health care system in the coming decades. About 10 per cent of the New Zealand population is affected by chronic kidney disease (CKD), with a higher incidence in Maori, Pacific, Asian and Indian groups. (1) The number of people receiving dialysis increased by eight per cent between 2008 and 2009, with the highest increase in older adults. (2) Risk of CKD increases with age, diabetes, cardiovascular disease, obesity or hypertension, smoking and a family history of CKD. (3) The commonest cause of CKD in this country is diabetes. There is an increased risk of developing diabetic nephropathy and CKD with prolonged hyperglycaemia, hypertension, smoking, Maori, Pacific or Asian ethnicity, dyslipidaemia or retinopathy. (4)

Acute renal failure or acute kidney injury (AKI) can occur following ischaemic or immune/infectious insult to the kidney. About four per cent of patients admitted to intensive care units develop AKI, and the mortality rate for these is greater than 60 per cent. (5) For general hospital populations, AKI incidence can be as high as 18 per cent, with a mortality rate of 30-60 per cent. (6) Following recovery from AKI, approximately 12 per cent of patients require ongoing dialysis and up to 30 per cent develop CKD. (6) THE ROLE OF THE KIDNEY

The ability of the kidneys to filter, reabsorb and secrete water, waste molecules and electrolytes determines the composition of both the body's extracellular fluid and the urinary filtrate. The kidneys receive 25 per cent of the cardiac output and plasma is filtered through the glomerular basement membrane at the rate of about 120ml/minute. Of this, all but l-2ml/minute is reabsorbed.

The glomerular filtration rate (GFR) of plasma is determined by the filtration pressure. Blood enters the glomerulus through the afferent arteriole and exits via the efferent arteriole. These two blood vessels are subject to neural, hormonal and intrinsic control mechanisms that maintain filtration pressure across a wide range of systemic blood pressure values. Dilation of the afferent arteriole or constriction of the efferent arteriole will increase GFR.

The purpose of glomerular filtration is to remove metabolic waste from the plasma, and to balance extracellular electrolyte and hydrogen ion concentrations (see figure 1, above). In this process, non-waste contents such as glucose and amino acids are reabsorbed. The structure of the glomerular filtration membrane is such that only small molecules and water can freely cross from the blood stream into the Bowman's capsule to form the glomerular filtrate: proteins and blood cells are retained in the plasma.

Excretion of waste

Creatinine is a waste product of muscle metabolism, and is released from skeletal muscle at a fairly constant rate. Creatinine is filtered at the glomerulus but does not get reabsorbed by the renal tubules, so the amount in the blood and urine is a measure of GFR. Rising creatinine concentration in the plasma indicates decreased glomerular filtration.

Serum creatinine levels are used to determine an estimated glomerular filtration rate (eGFR), but this can be subject to error, related to age, variations in body weight and composition, low protein (vegan) diet and in acute renal failure. It has not been validated as a measure outside the North American population, so may not accurately reflect GFR in Maori, Pacific or ethnic minorities. Also, there is little increase in plasma creatinine until up to 50 per cent of renal function has been lost, so early stages of renal impairment are not readily detected by this method. (1,3)

Urea is a by-product of protein metabolism. Nitrogen and ammonia, formed during the breakdown of proteins in the liver, are converted to urea. Urea is filtered at the glomerulus and then reabsorbed and secreted by the renal tubules. Blood urea nitrogen (BUN) is a measure of renal function: rising levels indicate reduced GFR and slow flow through the renal tubules (allowing more of the urea to be reabsorbed). However, BUN also varies with hydration status, dietary intake of protein and catabolic states in the body, such as following surgery or trauma.

Regulation of ions

Potassium handling via the kidneys is essential to the tight regulation of extracellular concentration, at about4.8mmol/L. Differences in potassium concentration between intracellular and extracellular fluids determine the resting membrane potential of all excitable cells within the body. Minor alterations in potassium concentration may be lethal.

Potassium is filtered at the glomerulus and largely reabsorbed in the proximal convoluted tubules. Potassium is then secreted into the urinary filtrate in the distal convoluted tubules (DCT). The extent of potassium loss depends on the concentration gradient across the tubule walls. Rapid flow of highly dilute filtrate will cause increased loss of potassium, while low plasma potassium concentration will decrease secretion. Aldosterone is released in response to high plasma concentrations of potassium and increases the rate of potassium secretion in the DCT.

Hydrogen ions also influence the secretion of potassium, linking pH and potassium balance. During acidosis, hydrogen ions move into the cells of the DCT in exchange for potassium, thus decreasing their intracellular potassium levels. The DCT cells react as if potassium in the body is low, and decrease secretion of potassium into the urinary filtrate, leading to hyperkalemia. The opposite occurs in alkalosis, where potassium moves into the cells, triggering increased secretion into the urinary filtrate and hypokalemia. (7)

The kidney has a complex mechanism for the excretion and buffering of excess hydrogen ions, thus maintaining acid-base balance in the body. Filtered bicarbonate is reabsorbed, while hydrogen ions are actively secreted and buffered with phosphate and ammonia. Bicarbonate reabsorption involves the formation of new bicarbonate molecules within the cells lining the tubules and is also affected by sodium and potassium exchanges in these cells. In renal failure, the inability of the cells to reabsorb filtered bicarbonate may lead to acidosis.

Renin-angiotensin-atdosterone system (RAAS)

Renal secretion of renin activates the renin-angiotensin-aldosterone pathway, leading to hormonal regulation of water and sodium in the extracellular fluid, and to maintenance of blood pressure via this and vasoconstrictive mechanisms (see fig 1).

Renin release is stimulated by hypovolaemia, hypotension or decreased sodium in the filtrate passing through the distal tubules. The classical pathway involves activation of angiotensinogen to angiotensin I by renin, and conversion of angiotensin I to angiotensin II by angiotensin-converting enzyme (ACE). Angiotensin II, acting via receptors, triggers vasoconstriction and increased retention of sodium and water, enhanced by release of aldosterone. Angiotensin II directly increases glomerular filtration pressure by causing constriction of the efferent arterioles. (7)

The RAAS also affects endothelial cell function throughout the body, triggering vascular remodelling, hypertrophy, increased oxidative stress, inflammation, atherogenesis and thrombosis. Inappropriate activation of RAAS in CKD causes ongoing renal hypertension, damaging the glomerular basement membrane, and inducing a chronic inflammatory state in the body, contributing to the many systemic effects of CKD.

The kidneys also regulate other body functions (see fig 1). Activation of vitamin D by the kidneys regulates calcium and phosphate metabolism and also affects immune function. Secretion of erythropoietin by the kidney regulates the synthesis of red blood cells; loss of this function is a major issue for people with CKD.

The kidney is the major site of excretion for drugs and their metabolites and other foreign substances. Impaired renal function can have a profound impact on the duration of action and potential toxicity of many drugs, particularly those excreted in their active form, eg penicillin.

RENAL INJURY

Regardless of the cause of renal injury, damage to the glomerulus leads to a sequence of events that, if allowed to progress, culminates in renal failure. This process may be acute, leading to abrupt loss of renal function, or more insidious, where chronic damage occurs over a number of years and renal failure is well advanced before it is detected. Figure 2 (p22) shows the sequence of events occurring in the nephrons when the glomerulus suffers injury.

Acute kidney injury (AKI)

AKI is a rapid decline in renal function leading to failure in fluid, electrolyte and acid-base homeostasis. Urine output falls below 0.5ml/kg/ hour for longer than six hours and serum creatinine levels increase. (8) The causes of AKI can be pre-renal, intrinsic or post-renal. Pre-renal causes generally arise due to hypoperfusion of the nephrons due to shock, heart failure, hypotension, dehydration, hypovolvaemia or renal arterial stenosis, which all decrease renal blood flow and may trigger renal failure.

These conditions may also cause ischaemia of the renal tubules, triggering acute tubular necrosis, a form of intrinsic AKI. Other forms of intrinsic AKI occur with nephrotoxic drugs (eg aminoglycosides such as gentamycin) or contrast media and the presence of endogenous nephrotoxic substances, eg haeme-pigment in rhabdomyolysis (abnormal breakdown of muscle, an adverse effect of statins). The risk of intrinsic AKI increases with age, presence of diabetes or concurrent CKD.

One of the hallmarks of acute tubular necrosis is the loss of ability to concentrate urine. As urinary filtrate travels through the collecting ducts, it normally encounters a highly concentrated interstitial zone in the renal medulla that draws water from the urinary filtrate by osmosis. Establishment of this zone is dependent on the orchestrated movement of water and electrolytes from the filtrate as it travels through the loop of Henle, and on adequate blood flow through the renal capillaries. If the loop of Henle is unable to generate this osmotic gradient, urinary filtrate cannot be concentrated, so the person with acute tubular necrosis will produce dilute urine despite being oliguric (producing low amount of urine). Once the recovery phase begins, the restoration of glomerular filtrate may occur prior to re-establishment of tubule function. Resultant polyuria increases the risk of hypovolemia and further hypoxic injury to the kidney.

[FIGURE 2 OMITTED]

Glomerulonephritis is a form of intrinsic injury that occurs where antibody-antigen complexes either form or are deposited within the glomerulus. These damage the glomerular basement membrane and trigger the sequence of events shown in figure 2. Streptococcal infections (impetigo, strep throat) may trigger AKI in children seven to 10 days after infection, but this condition can also arise with other bacteria or viral infections (acute post-infectious glomerulonephritis). Other forms of immune-triggered AKI may occur in immune disorders such as systemic lupus erythematosis. (7)

Post-renal injury may arise where there is prolonged obstruction to the flow of urine or filtrate, causing a build-up of pressure in the renal tubules and negation of the filtration gradient from glomerulus into the Bowman's capsule. This, in turn, triggers renal afferent arteriolar vasoconstriction, reducing blood flow through the glomerulus and renal tubule. Sloughing of dead tubule cells from an already damaged kidney can cause obstruction to flow, increasing the damage from pre-renal or intrinsic causes.

Recovery depends on rapid correction of the underlying causative factor(s). Once renal blood flow is restored, surviving nephrons are able to compensate by increasing their filtration rate (hyperfiltration) and, over time, their size (hypertrophy). However, if the number of functional nephrons is too low, this hyperfiltration and hypertrophy continue leading to a cycle of sclerosis and further nephron loss. Eventually, despite initial recovery of function, the kidney may fail completely. (6)

Chronic kidney disease

Loss of renal function over a prolonged period (months to years) is now described as CKD, rather than chronic renal failure. Stages of CKD range from kidney damage with normal renal function, through to end-stage renal disease (ESRD). (9) Underlying causes of CKD vary--diabetes being the most common. Hypertension, glomerulonephritis, reflux nephropathy and polycystic kidney disease are other causes. Regardless of initiating events, CKD progresses due to glomerular hypertension, glomerulosclerosis, compensatory (and ultimately pathological) hyperfiltration and hypertrophy, and tubular inflammation and fibrosis. Symptoms of CKD do not normally manifest until renal function decreases to less than 25 per cent.7 People with CKD are particularly vulnerable to AKI, the highest risk being during episodes in hospital.

CONSEQUENCES OF RENAL DYSFUNCTION

Adverse consequences of AKI depend on the phase of the illness: initiation (damage is in progess), maintenance (renal injury is established) and recovery. Generally the first two phases are oliguric, and polyuria occurs during the recovery phase. In advanced CKD, oliguric effects predominate. Fluid and electrolyte disturbances (including hypertension, oedema and heart failure), uraemia, anaemia and infection may all have a bad effect on the outcomes for patients.

Fluids and electrolytes

Increasing plasma potassium and sodium, and water retention in the oliguric phase of AKI cause disruption to fluid and electrolyte balance throughout the body. Hyperkalaemia can induce life-threatening cardiac dysrhythmias--ventricular tachycardia or fibrillation, bradycardia, complete heart block or asystole. Also, possible neuromuscular dysfunction can lead to respiratory failure. Hyperkalaemia is treated with insulin/ glucose infusion, ion exchange resin (calcium resonium or resonium A) or, if severe, dialysis. (10) As diuresis sets in with the recovery phase, the risk of hypokalaemia increases.

Abnormal activation of the RAAS and reduced sodium excretion affect body water balance. Oedema and congestive heart failure develop due to fluid retention. Fluid losses in the recovery phase of AKI may cause dehydration and further renal injury.

Hyponatremia may occur with some forms of CKD and during the recovery phase of AKI. It must be corrected slowly due to the impact of rapidly altered osmotic pressures on the brain.

[FIGURE 3 OMITTED]

ESRD can induce severe metabolic acidosis due to loss of renal compensatory mechanisms and bicarbonate handling.

Uraemia

Accumulation of nitrogenous and other toxic wastes leads to development of gastrointestinal symptoms (anorexia, nausea, vomiting, cramps). As BUN increases, neurological symptoms of lethargy, confusion and seizures may develop. Uraemia causes platelet dysfunction that can lead to life-threatening haemorrhage; (10) it also impairs immune function, increasing the risk of developing infections, especially pneumonia. Infection is the commonest cause of morbidity and death for patients with AKI (10) and the second most common, after cardiovascular disease, for CKD. (1)

Other effects of uraemia include pruritis, peripheral neuropathy, mouth ulcers, pancreatitis, sexual dysfunction and infertility.

Anaemia

Red blood cell production may be reduced due to loss of erythropoietin (EPO) secretion from the damaged kidneys. Bone marrow becomes less sensitive to the action of EPO, possibly due to chronic systemic inflammation. (3) Blood loss may also occur via the kidneys or due to haemorrhage. Water retention causes a dilution anaemia.

Hypertension

Water and sodium retention increase blood volume and thus blood pressure. Abnormal activation of the reninangiotensin pathway increases aldosterone secretion, so that sodium retention is increased in remaining

functional nephrons. Angiotensin II causes vasoconstriction, including of the afferent arterioles, increasing glomerular hypertension and damage.

Cardiac disease

The majority of people with CKD will die from cardiovascular disease: patients on dialysis are 10-20 times more likely to die of cardiovascular disease than the general population. (3,11) CKD is an independent risk factor for cardiovascular disease, and cardiovascular disease increases risk of CKD. Therapies aimed at reducing cardiovascular risk will slow progression of CKD. Underlying mechanisms in the development of cardiovascular disease with CKD include hypertension, dyslipidaemia, abnormal endothelial cell function and chronic inflammation.

Bone changes

Reduced activation of vitamin D, combined with phosphate retention, cause hyperparathyroidism and hypocalcaemia. Osteomalacia and osteitis fibrosa ensue, with bone pain and increased risk of fractures. Persistent elevated parathyroid hormone also induces soft tissue calcification and cardiovascular disease. (7)

Malnutrition

Weight loss in renal disease is not solely due to reduced food intake. Loss of protein in the urine and a catabolic metabolic state lead to reduced plasma proteins and muscle wasting. Loss of plasma proteins increases the development of oedema.

DIET IN RENAL DISEASE

Restricting protein intake in CKD can delay progression of the disease and reduce adverse cardiovascular effects and uraemia (12). While those with CKD generally suffer from low serum albumin, this reduction is probably more due to loss of protein through the damaged kidneys, metabolic acidosis, dialysis and on-going inflammation, rather than malnutrition. (12)

A low-protein diet reduces production of nitrogenous wastes, reducing renal damage, inflammation and gastrointestinal symptoms. Low-protein diets are also associated with reduced sodium, phosphate and acid intake, reducing development of hypertension, hyperphosphataemia and acidosis. Very low protein diets must be accompanied by supplements of essential amino acids and ketoacids.

Sticking to restrictive diets long-term is difficult for many people and there is an associated risk of malnutrition, increased in the presence of underlying disease. Research evidence is not conclusive on the effectiveness of low-protein diets, particularly in early stages of CKD and this intervention is not recommended until late in the disease. (13,14) Malnutrition may require high-energy dietary interventions. Of particular concern is where calorie deficits increase the use of protein as an energy source, increasing production of nitrogenous waste. Reduced appetite and other gastrointestinal effects of uraemia can contribute to this state. The high risk of cardiovascular disease for people with CKD affects the types of protein and carbohydrates that should be included in the diet. Specialist renal dieticians are an essential component of care for people with CKD.

TREATMENT OF CKD

Figure 3 (see p23) illustrates the progression of CKD and the nature of interventions provided at each stage. Screening for, and purposeful management of, modifiable risk factors can prevent, delay and sometimes reverse the onset of the disease.

Early renal damage is indicated by the presence of persistent microalbuminuria/ proteinuria or haematuria, and abnormal urine microscopy or renal defects on ultrasound or radiology. At this stage, giving drugs that prevent the actions of angiotensin II has been shown to delay further deterioration in renal function. (1)

ACE-inhibitors (eg lisinopril, enalapril) are the first-line drugs used or, if these are not well tolerated, angiotensin II receptor blockers (ARBs) such as losartan or candesartan. By inhibiting the actions of angiotensin II, these drugs reduce afferent arteriolar vasoconstriction, decreasing glomerular hypertension and its consequences on glomerular structure and function. The systemic chronic inflammatory effects of angiotensin II are also reduced. (15) The effects of RAAS blockade are enhanced when sodium intake is restricted. (16)

As renal function deteriorates and GFR declines, the focus of treatment shifts to include protection of remaining renal function. The increased vulnerability of the failing kidneys to injury is of prime concern. All medications should be reviewed for their potential to damage the kidneys. Fluid and electrolyte management becomes especially important during any form of health intervention, eg surgery. Prevention of infection is also essential and vaccination against seasonal influenza and pneumococcus should be encouraged. (1,3)

Decisions on kidney transplant need to be made as ESRD approaches. In 2010, 2378 patients were receiving dialysis in New Zealand and there were 1442 people with functioning transplants. (17)

Haemodialysis, peritoneal dialysis and kidney transplant are expensive, with variable outcomes for patients. Survival rates following transplantation are about 90 per cent at one year, dropping to 40 per cent at 10 years. (3) Survival rates with dialysis are substantially lower. Overall survival rates on haemodialysis (HD) and peritoneal dialysis (PD) are similar, although older patients with diabetes have worse outcomes with peritoneal dialysis. (18)

Dialysis involves the exchange of substances between the blood and another fluid (dialysate) by diffusion and ultrafiltration across a semi permeable membrane. In the case of PD, this is the peritoneal membrane surrounding the abdominal organs. With haemodialysis, an artificial membrane is used and blood must be extracted and returned to the body.

CONCLUSION

The kidneys provide complex and essential support to the maintenance of homeostasis of fluids and electrolytes, blood pressure and acid-base balance. They are also responsible for the removal of waste products of metabolism and drugs from the body. Renal failure is manifested across this wide range of functions and offers an interesting challenge to those providing care for people with AKI or CKD. Understanding the pathophysiology involved allows nurses to deliver optimal care and support to these patients.

* For this article's references, go to CPD4nurses.co.nz and click under the 'News' link.

LEARNING OUTCOMES

After reading this article and completing the accompanying online learning activities, you should be able to:

* Outline the roles of the kidney in maintaining homeostasis.

* Describe the causes and consequences of acute kidney injury.

* Describe the course of chronic kidney disease and its progression to end-stage renal disease.

* Discuss common measurements of renal function.

Georgina Casey, RN, BSc, PGDipSci, MPhil (nursing), is the director of CPD4nurses.co.nz. She has an extensive background in nursing education and clinical experience in a wide variety of practice settings.
Table 1. Advantages and disadvantages of haemodialysis and
peritoneal dialysis ... (19)

                HAEMODIALYSIS                    PERITONEAL DIALYSIS

Advantages      High clearance of solutes        Less risk of
                allows intermittent treatment.   hypotension than HD.
                Easier to detect and manage      Patient-controlled.
                under dialysis.                  Less restriction of
                                                 mobility during
                                                 sessions. No
                                                 anticoagulation
                                                 required.

Disadvantages   Loss of patient control over     Risk of malnutrition
                dialysis.                        due to abdominal
                                                 fullness and loss of
                                                 larger solutes in
                                                 PD.

                Loss of mobility during          High risk of
                dialysis.                        peritonitis.

                Risk of hypotension.             Risk of catheter
                Risk of infection or             malfunction or
                thrombosis in vascular           insertion site
                access site.                     infection.
                Risk associated with need for
                anticoagulant therapy.           Lower clearance of
                Increased incidence of           solutes than HD so
                anaemia.                         more frequent
                                                 dialysis required.

                                                 Discomfort, leakage
                                                 and burnout may
                                                 reduce compliance.
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Title Annotation:CONTINUING PROFESSIONAL DEVELOPMENT
Author:Casey, Georgina
Publication:Kai Tiaki: Nursing New Zealand
Article Type:Disease/Disorder overview
Geographic Code:8NEWZ
Date:May 1, 2012
Words:3621
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