CHRONIC KIDNEY DISEASE

Essentials of Diagnosis

Progressive azotemia over months to years.

Symptoms and signs of uremia when nearing end-stage disease.

Hypertension in the majority.

Isosthenuria and broad casts in urinary sediment are common.

Bilateral small kidneys on ultrasound are diagnostic.

General Considerations
Chronic kidney disease affects up to 20 million Americans, or one in nine adults. Most are unaware of the condition because they remain asymptomatic until the disease has significantly progressed. The National Kidney Foundation’s staging system helps clinicians formulate practice plans (Table 22–5). Over 70% of cases of late-stage chronic kidney disease are due to diabetes mellitus or hypertension. Glomerulonephritis, cystic diseases, and other urologic diseases account for another 12%, and 15% of patients have other or unknown causes.

Table 22–6. Major causes of chronic renal failure.

Glomerulopathies
Primary glomerular diseases:
Focal and segmental glomerulosclerosis
Membranoproliferative glomerulonephritis
IgA nephropathy
Membranous nephropathy
Secondary glomerular diseases:
Diabetic nephropathy
Amyloidosis
Postinfectious glomerulonephritis
HIV-associated nephropathy
Collagen-vascular diseases
Sickle cell nephropathy
HIV-associated membranoproliferative glomerulonephritis
Tubulointerstitial nephritis
Drug hypersensitivity
Heavy metals
Analgesic nephropathy
Reflux/chronic pyelonephritis
Idiopathic
Hereditary diseases
Polycystic kidney disease
Medullary cystic disease
Alport’s syndrome
Obstructive nephropathies
Prostatic disease
Nephrolithiasis
Retroperitoneal fibrosis/tumor
Congenital
Vascular diseases
Hypertensive nephrosclerosis
Renal artery stenosis

Chronic kidney disease is rarely reversible and leads to a progressive decline in renal function. This occurs even after an inciting event has been removed. Reduction in renal mass leads to hypertrophy of the remaining nephrons with hyperfiltration. The GFR in these nephrons is transiently at supranormal levels. These adaptations place a burden on the remaining nephrons and lead to progressive glomerular sclerosis and interstitial fibrosis, suggesting that hyperfiltration may worsen renal function. However, decreased renal mass in kidney donors is not associated with chronic renal failure.
Clinical Findings
SYMPTOMS AND SIGNS
The symptoms of chronic kidney disease often develop slowly and are nonspecific (Table 22–7). Individuals can remain asymptomatic until renal failure is far advanced (GFR < 10–15 mL/min). Manifestations include fatigue, weakness, and malaise. Gastrointestinal complaints, such as anorexia, nausea, vomiting, a metallic taste in the mouth, and hiccups are common. Neurologic problems include irritability, difficulty in concentrating, insomnia, subtle memory defects, restless legs, and twitching. Pruritus is common and difficult to treat. As uremia progresses, decreased libido, menstrual irregularities, chest pain from pericarditis, and paresthesias can develop. Symptoms of drug toxicity—especially for drugs eliminated by the kidney—increase as renal clearance worsens.
On physical examination, the patient appears chronically ill. Hypertension is common. The skin may be yellow, with signs of easy bruisability. Rarely seen in the dialysis era is uremic frost, a cutaneous reflection of ESRD. Uremic fetor is the characteristic fishy odor of the breath. Cardiopulmonary signs may include rales, cardiomegaly, edema, and a pericardial friction rub. Mental status can vary from decreased concentration to confusion, stupor, and coma. Myoclonus and asterixis are additional signs of uremic effects on the central nervous system.
The term "uremia" is used for this clinical syndrome, but the exact cause remains unknown. BUN and serum creatinine are considered markers for unknown toxins, with parathyroid hormone (PTH) possibly one such toxin.
In any patient with renal failure, it is important to identify and correct all possibly reversible causes. Urinary tract infections, obstruction, extracellular fluid volume depletion, nephrotoxins, hypertension, and congestive heart failure should be excluded (Table 22–8). Any of the above can worsen underlying chronic renal failure.
LABORATORY FINDINGS
The diagnosis of renal failure is made by documenting elevations of the BUN and serum creatinine concentrations. Further evaluation is needed to differentiate between acute and chronic renal failure. Evidence of previously elevated BUN and creatinine, abnormal prior urinalyses, and stable but abnormal serum creatinine on successive days is most consistent with a chronic process. It is helpful to plot the inverse of serum creatinine (1/SCr) versus time if three or more prior measurements are available; this estimates time to ESRD (Figure 22–1: illustration). If the slope of the line acutely declines, new causes of renal failure should be excluded as outlined above. Anemia, metabolic acidosis, hyperphosphatemia, hypocalcemia, and hyperkalemia can occur with both acute and chronic renal failure. The urinalysis shows isosthenuria if tubular concentrating and diluting ability are impaired. The urinary sediment can show broad waxy casts as a result of dilated, hypertrophic nephrons.
IMAGING
The finding of small echogenic kidneys bilaterally (< 10 cm) by ultrasonography supports a diagnosis of chronic renal failure, though normal or even large kidneys can be seen with chronic renal failure caused by adult polycystic kidney disease, diabetic nephropathy, HIV-associated nephropathy, multiple myeloma, amyloidosis, and obstructive uropathy. Radiologic evidence of renal osteodystrophy is another helpful finding, since x-ray changes of secondary hyperparathyroidism do not appear unless parathyroid levels have been elevated for at least 1 year. Evidence of subperiosteal reabsorption along the radial sides of the digital bones of the hand confirms hyperparathyroidism (see x-ray).
Complications
HYPERKALEMIA
Potassium balance generally remains intact in chronic renal failure until the GFR is less than 10–20 mL/min. However, certain states pose an increased risk of hyperkalemia at higher GFRs. Endogenous causes include any type of cellular destruction such as hemolysis and trauma, hyporeninemic hypoaldosteronism (type IV renal tubular acidosis, seen particularly in diabetes mellitus), and acidemic states (0.6 mEq/L elevation in K+ for each 0.1 unit decrease in pH). Exogenous causes include diet (eg, citrus fruits and salt substitutes containing potassium) and drugs that decrease K+ secretion (amiloride, triamterene, spironolactone, NSAIDs, ACE inhibitors) or block cellular uptake (
-blockers).
Treatment of acute hyperkalemia involves cardiac monitoring, intravenous calcium chloride or gluconate, insulin administration with glucose, bicarbonate, and an orally or rectally administered ion exchange resin (sodium polystyrene sulfonate). The resin exchanges sodium for potassium and can administer a significant sodium load to a patient.
-Agonists such as albuterol may also be used in acute cases. Chronic hyperkalemia is best treated with dietary potassium restriction (2 g/d) and sodium polystyrene sulfonate when necessary. The usual dose is 15–30 g once a day in juice or sorbitol.
ACID–BASE DISORDERS
Damaged kidneys are unable to excrete the 1 mEq/kg/d of acid generated by metabolism of dietary proteins. The resultant metabolic acidosis is primarily due to loss of renal mass. This limits production of ammonia (NH3) and limits buffering of H+ in the urine. (Other causes include decreased filtration of titratable acids such as sulfates and phosphates, decreased proximal tubular bicarbonate resorption, and decreased renal tubular hydrogen ion secretion.) Although patients with chronic renal failure are in positive hydrogen ion balance, the arterial blood pH is maintained at 7.33–7.37 and serum bicarbonate concentration rarely falls below 15 mEq/L. The excess hydrogen ions are buffered by the large calcium carbonate and calcium phosphate stores in bone. This contributes to the renal osteodystrophy of chronic renal failure described below.
The serum bicarbonate level should be maintained at greater than 21 mEq/L according to recently published national guidelines. Alkali supplements include sodium bicarbonate, calcium bicarbonate, and sodium citrate. Citrate salts increase the absorption of dietary aluminum and should be avoided in patients exposed to aluminum. Administration should begin with 20–30 mmol/d of alkali divided into two doses per day and titrated as needed.
CARDIOVASCULAR COMPLICATIONS
Long-term complications of chronic kidney disease include a high risk of morbidity and mortality of cardiovascular disease in comparison to the general population. Mortality due to a cardiovascular cause accounts for 45% of all deaths of patients receiving dialysis. The precise biologic mechanisms for this are unclear but may have to do with the uremic milieu, underlying coexistent comorbidities, and a hesitancy to perform investigative procedures in patients with chronic kidney disease.
Hypertension
As renal failure progresses, hypertension due to salt and water retention usually develops. Hyperreninemic states and exogenous erythropoietin administration can also exacerbate hypertension. Hypertension is the most common complication of ESRD and must be meticulously controlled. Failure to do so can accelerate the progression of renal damage.
Control of hypertension can be achieved with salt and water restriction, weight loss if indicated, and pharmacologic therapy. The ability of the kidney to adjust to variations in sodium and water intake becomes limited as renal failure progresses. An elevated sodium chloride intake leads to congestive heart failure, edema, and hypertension, whereas low salt intake leads to volume contraction and hypotension. A mildly decreased salt diet (4 g/d) can be started, and salt intake should be reduced to 2 g/d if hypertension persists. Initial drug therapy can include ACE inhibitors or angiotensin II receptor blockers (if serum potassium and GFR permit), calcium channel-blocking agents, diuretics, and
-blocking agents. The adjunctive drugs that are often needed (eg, clonidine, hydralazine, minoxidil) reflect the difficulty of achieving and maintaining hypertensive control in these patients. Goal blood pressure for patients with chronic kidney disease is less than 130/80 mm Hg.
Pericarditis
With uremia, pericarditis may develop. The cause is believed to be retention of metabolic toxins. Symptoms include chest pain and fever. Pulsus paradoxus can be present. A friction rub may be auscultated, but the lack of a rub does not rule out a significant pericardial effusion. Chest radiography will show an enlarged cardiac silhouette, and an ECG will show characteristic findings as explained in Cardiology. Cardiac tamponade can occur; these patients have signs of poor cardiac output (see Video), with jugular venous distention and lungs clear to auscultation. Pericarditis is an absolute indication for initiation of hemodialysis.

Video

Uremic pericardial effusion. (Courtesy of E Foster.)

Congestive heart failure
Patients with ESRD tend toward a high cardiac output. They often have extracellular fluid overload, shunting of blood through an arteriovenous fistula for dialysis, and anemia. In addition to hypertension, these abnormalities cause increased myocardial work and oxygen demand. Patients with chronic kidney disease may also have accelerated rates of atherosclerosis. All of these factors contribute to left ventricular hypertrophy and dilation, present in 75% of patients starting dialysis. PTH may also play a role in the pathogenesis of the cardiomyopathy of renal failure.
Water and salt intake should be controlled in patients who are oliguric or anuric. Diuretics are of value, though certain thiazides are ineffective when the GFR is less than 10–15 mL/min. Loop diuretics are commonly used, and higher doses are required as renal function declines. Digoxin should be used with caution since it is excreted by the kidney. The proved efficacy of ACE inhibitors in congestive heart failure holds true for patients with chronic renal failure. Despite the risks of hyperkalemia and worsening renal function, ACE inhibitors can be used for patients with a serum creatinine greater than 3 mg/dL with close supervision. Along with angiotensin II receptor blockers, ACE inhibitors have been shown to slow the progression to ESRD, even for patients with advanced chronic kidney disease. (See above section regarding treatment of proteinuria.) Once a patient is receiving dialysis, these risks become less relevant. When an ACE inhibitor or ARB drug is initiated, patients should have serum creatinine and potassium checked within 5–14 days.
HEMATOLOGIC COMPLICATIONS
Anemia
The anemia of chronic renal failure is characteristically normochromic and normocytic. It is due primarily to decreased erythropoietin production, which becomes clinically significant when GFR falls below 20–25 mL/min. Many patients are iron deficient as well. Low-grade hemolysis and blood loss from platelet dysfunction or hemodialysis play an additional role.
Recombinant erythropoietin or darbepoetin is used in patients whose hematocrits are less than 33% if no other causes are present. The effective dose can vary; the starting dose of erythropoietin is 50 units/kg (3000–4000 units/dose) once or twice a week. Darbepoetin is started at 0.45 mcg/kg once weekly and can be administered every 2–4 weeks. Both medications should be titrated to a hemoglobin of 11–13 g/dL according to national guidelines, but studies suggested that an upper limit of 12 g/dL might be more appropriate for optimal safety. These agents can be given intravenously (eg, in the hemodialysis patient) or subcutaneously (eg, in any predialysis or dialysis patient). Subcutaneous administration is preferable to intravenous administration because it requires a 33% lower dose for the same effect. Iron stores must be adequate to ensure response. Hemodialysis patients typically require 50–200 mg intravenous iron each month due to expected blood loss at dialysis. Other patients with serum ferritin less than 100 ng/mL or iron saturation less than 20% should also receive iron supplementation. Depending on the clinical situation, iron therapy should be withheld if the serum ferritin is greater than 800 ng/mL. Oral therapy with ferrous sulfate, 325 mg once daily to three times daily, is adequate but not always well tolerated, and gut absorption of iron is impaired in uremic patients. Ferrous fumarate is the best-accepted formulation, and intravenous iron may be used in dialysis patients. Hypertension is a complication of epoetin alfa therapy in about 20% of patients. It develops more abruptly in the patients with the lowest hematocrit values at initiation of therapy, and in those with the greatest rate of rise in hemoglobin. The dosage may require adjustment, or antihypertensive drugs may need to given. Hemoglobin levels should rise no more than 1 g/dL every 3–4 weeks.
Coagulopathy
The coagulopathy of chronic kidney disease is mainly caused by platelet dysfunction. Platelet counts are only mildly decreased, but the bleeding time is prolonged. Platelets show abnormal adhesiveness and aggregation. Clinically, patients can have petechiae, purpura, and an increased tendency for bleeding during surgery.
Treatment is required only in patients who are symptomatic. Raising the hematocrit to 30% can reduce bleeding time in many patients. Desmopressin (25 mcg intravenously every 8–12 hours for two doses) is effective and often used in preparation for surgery. It causes release of factor VIII bound to von Willebrand’s factor from endothelial cells. Conjugated estrogens, 0.6 mg/kg diluted in 50 mL of 0.9% sodium chloride infused over 30–40 minutes daily, or 2.5–5 mg orally for 5–7 days, have an effect for several weeks. Dialysis improves the bleeding time but does not normalize it. Peritoneal dialysis is preferable to hemodialysis because the latter requires heparin to prevent clotting in the dialyzer. Cryoprecipitate (10–15 bags) is rarely used and lasts less than 24 hours.
NEUROLOGIC COMPLICATIONS
Uremic encephalopathy does not occur until GFR falls below 10–15 mL/min. Encephalopathy may be due to tertiary hyperparathyroidism, where an elevated PTH level or, rarely, hypercalcemia, can be the culprit. PTH may be one of the uremic toxins. Symptoms begin with difficulty in concentrating and can progress to lethargy, confusion, and coma. Physical findings include nystagmus, weakness, asterixis, and hyperreflexia. These symptoms and signs may improve after initiation of dialysis.
Neuropathy is found in 65% of patients who receive dialysis or who will need it soon but not until GFR is 10% of normal. Peripheral neuropathies manifest themselves as sensorimotor polyneuropathies (stocking and glove distribution) and isolated or multiple isolated mononeuropathies. Patients can have restless legs, loss of deep tendon reflexes, and distal pain. The earlier initiation of dialysis may prevent peripheral neuropathies, and the response to dialysis is variable. Other neuropathies result in impotence and autonomic dysfunction.
DISORDERS OF MINERAL METABOLISM
The disorders of calcium, phosphorus, and bone are referred to as renal osteodystrophy (see illustration). The most common disorder is osteitis fibrosa cystica—the bony changes of secondary hyperparathyroidism. This affects ~ 50% of patients nearing ESRD. As GFR decreases below 25% of normal, phosphorus excretion is impaired. Hyperphosphatemia leads to hypocalcemia, stimulating secretion of PTH, which has a phosphaturic effect and normalizes serum phosphorus. This continuous process leads to markedly elevated PTH levels and high bone turnover with osteoclastic bone resorption and subperiosteal lesions. Metastatic calcifications, such as tumoral calcinosis, can occur. Radiographically, lesions are most prominent in the phalanges and lateral ends of the clavicles.
Osteomalacia is a form of renal osteodystrophy with low bone turnover (affecting
10% of patients nearing ESRD). With worsening renal function, there is decreased renal conversion of 25-hydroxycholecalciferol to the 1,25-dihydroxy form. Gut absorption of calcium is diminished, leading to hypocalcemia and abnormal bone mineralization. Deposition of aluminum in bone can also lead to osteomalacia. Elevated aluminum levels are seen in patients after years of chronic aluminum hydroxide administration for phosphorus binding. This entity is seen with decreasing frequency because aluminum-based binders are used less in the chronic setting and water used for hemodialysis is now cleared of aluminum.
Adynamic bone disease is a disorder of low bone turnover. More than 25% of patients nearing ESRD show evidence of minimal osteoid and decreased or absent bone remodeling. Its frequency is increasing because of increased use of active vitamin D analogs, which suppress PTH production.
All of the above entities can cause bony pain and proximal muscle weakness. Spontaneous bone fractures can occur that are slow to heal. When the calcium-phosphorus product (serum calcium [mg/dL] x serum phosphate [mg/dL]) is above 60–70, metastatic calcifications are commonly seen in blood vessels, soft tissues, lungs, and myocardium. Treatment should begin with dietary phosphorus restriction to 1000 mg/d. Oral phosphorus-binding agents such as calcium carbonate or calcium acetate act in the gut and are given in divided doses three or four times daily with meals. These should be titrated to a serum calcium of less than 10 mg/dL (preventing hypercalcemia) and serum phosphorus of 2.7–4.6 mg/dL in patients with a GFR of 15–59 mL/min/1.73 m2 and serum phosphorus of 3.5–5.5 mg/dL in patients with a GFR of less than 15 mL/min/1.73 m2. Sevelamer and lanthanum carbonate are other phosphorus-binding agents that do not contain calcium; they are particularly useful in patients with hypercalcemia, although long-term effects are unknown. Aluminum hydroxide is an effective phosphorus binder but can cause osteomalacia and neurologic complications. It can be used in the acute setting for serum phosphorus greater than 7 mg/dL, but long-term use should be avoided. If aluminum levels are high, chelation with deferoxamine can be effective. Vitamin D or vitamin D analogs should be given with secondary hyperparathyroidism (iPTH more than two to three times normal) if phosphorus levels are less than 5.5 mg/dL and calcium less than 10 mg/dL. Vitamin D suppresses PTH and increases serum calcium and phosphorus levels; both need to be monitored closely to prevent hypercalcemia and hyperphosphatemia. If calcitriol is used, the dosage should be 0.25–0.5 mcg daily or every other day initially. Cinacalcet can be used if elevated serum phosphorus or calcium levels prohibit the use of vitamin D analogs. Cinacalcet is a calcimimetic agent that targets the calcium-sensing receptor on the chief cells of the parathyroid gland.
ENDOCRINE DISORDERS
Circulating insulin levels are higher because of decreased renal insulin clearance. Glucose intolerance can occur in chronic renal failure when GFR is less than 10–20 mL/min. Primarily, this is due to peripheral insulin resistance. Fasting glucose levels are usually normal or only slightly elevated. Therefore, patients can be either hyperglycemic or hypoglycemic depending on the predominant disturbance. Most commonly, diabetic patients require decreased doses of hypoglycemic agents.
Decreased libido and impotence are common in chronic renal failure. Men have decreased testosterone levels; women are often anovulatory. Despite a high degree of infertility, pregnancy can occur—particularly in women who are well dialyzed and well nourished. Therefore, contraception is advisable for women who do not wish to become pregnant.
Treatment
DIETARY MANAGEMENT
Every patient with chronic renal failure should be evaluated by a renal nutritionist. Specific recommendations should be made concerning protein, salt, water, potassium, and phosphorus intake.
Protein restriction
Experimental models have shown that protein restriction slows the progression to ESRD; however, this has not been consistently proved in clinical trials. The MDRD Study was meant to clarify the issue, but the results were inconclusive. A subsequent meta-analysis of five clinical trials did show a significant benefit but did not control for certain effects such as ACE inhibitor therapy. The benefits of protein restriction in slowing the rate of decline of GFR must be weighed against the risk of cachexia upon the institution of dialysis. Low serum albumin at the start of dialysis is one of the strongest predictors of mortality in this population. In general, protein intake should not exceed 1 g/kg/d, and if protein restriction proves to be beneficial, the level of restriction may be increased to 0.6–0.8 g/kg/d.
Salt and water restriction
In advanced renal failure, the kidney is unable to adapt to large changes in sodium intake. Intake greater than 3–4 g/d can lead to edema, hypertension, and congestive heart failure, whereas intake of less than 1 g/d can lead to volume depletion and hypotension. For the nondialysis patient approaching ESRD, 2 g/d of sodium is an initial recommendation. A daily intake of 1–2 L of fluid maintains water balance.
Potassium restriction
Restriction is needed once the GFR has fallen below 10–20 mL/min. Patients should receive detailed lists concerning potassium content of foods and should limit their intake to less than 50–60 mEq/d (2 g). Normal intake is about 100 mEq/d.
Phosphorus restriction
The phosphorus level should be kept below 4.6 mg/dL predialysis and below 5.5 mg/dL when on dialysis, with a dietary restriction of 800–1000 mg/d. Foods rich in phosphorus such as cola beverages, eggs, dairy products, and meat should be limited. Below a GFR of 20–30 mL/min, phosphorus binders are usually required. The treatment of hyperphosphatemia is discussed in the section on disorders of mineral metabolism.
Magnesium restriction
Magnesium is excreted primarily by the kidneys. Dangerous hypermagnesemia is rare unless the patient ingests medications high in magnesium or receives it parenterally. All magnesium-containing laxatives and antacids are relatively contraindicated in renal failure.
DIALYSIS
When conservative management of ESRD is inadequate, hemodialysis, peritoneal dialysis, and kidney transplantation are alternatives (see below). According to the Kidney Disease Outcomes Quality Initiative (KDOQI) guidelines, dialysis should be started when a patient has a GFR of 10 mL/min or serum creatinine of 8 mg/dL. Diabetic patients should start when the GFR reaches 15 mL/min or serum creatinine is 6 mg/dL. Other indications for dialysis include (1) uremic symptoms, such as pericarditis, encephalopathy, or coagulopathy; (2) fluid overload unresponsive to diuresis; (3) refractory hyperkalemia; (4) severe metabolic acidosis (pH < 7.20); and (5) neurologic symptoms such as seizures or neuropathy. Preparation for dialysis requires a team approach. Dietitians, social workers, psychiatrists, and transplant surgeons should be involved as well as primary care physicians and nephrologists. The patient and family need early counseling regarding the risks and benefits of therapy. The options of not starting or withdrawing dialysis should be discussed openly.
Hemodialysis
Hemodialysis requires a constant flow of blood along one side of a semipermeable membrane with a cleansing solution, or dialysate, along the other. Diffusion and convection allow the dialysate to remove unwanted substances from the blood while adding back needed components. Vascular access for hemodialysis can be accomplished by an arteriovenous fistula (the preferred method) or prosthetic graft. Indwelling catheters should be considered temporary measures. Native fistulas typically last longer than prosthetic shunts but require longer time (6–8 weeks or more after surgical construction) before they can be used. Infection, thrombosis, and aneurysm formation are complications seen more often in grafts than fistulas. Staphylococcus aureus is the most common infecting agent.
Patients typically require hemodialysis three times a week. Sessions last 3–5 hours depending on patient size, type of dialyzer used, and other factors. Periodic measurement of dialysis adequacy should determine the duration of treatment. Home hemodialysis is an option that is becoming less popular because of the need for a trained helper, large equipment, and costs. Nocturnal and daily hemodialysis are other forms of hemodialysis that offer improved outcomes in certain populations. Unfamiliarity with home hemodialysis and the financial impact with most current reimbursement schemes are currently limiting the availability of these modalities.
Peritoneal dialysis
With peritoneal dialysis, the peritoneal membrane is the "dialyzer." Fluids and solutes move across the capillary bed that lies between the visceral and parietal layers of the membrane into the dialysate. Dialysate enters the peritoneal cavity through a catheter. The most common kind of peritoneal dialysis is continuous ambulatory peritoneal dialysis (CAPD). Patients exchange the dialysate four to six times a day. Continuous cyclic peritoneal dialysis (CCPD) utilizes a cycler machine to automatically perform exchanges at night. The dialysate remains in the peritoneal cavity between exchanges. As with hemodialysis, actual peritoneal dialysis prescriptions are guided by adequacy measurements.
The percentage of dialysis patients using peritoneal dialysis has been decreasing over the past several years. Peritoneal dialysis permits greater patient autonomy; its continuous nature minimizes the symptomatic swings observed in hemodialysis patients; and poorly dialyzable compounds such as phosphates are better cleared, which permits less dietary restriction. The dialysate removes large amounts of albumin, and nutritional status must be closely watched.
The most common complication of peritoneal dialysis is peritonitis. Rates are as high as 0.8 episodes per patient-year. The patient can experience nausea and vomiting, abdominal pain, diarrhea or constipation, and fever. The dialysate can be cloudy and contain greater than 100 white cells/mcL of which over 50% are polymorphonuclear neutrophils. S aureus is the most common infecting organism.
The total costs of peritoneal dialysis and hemodialysis are approximately the same. Equipment expenses are less for peritoneal dialysis, but the costs of peritonitis are high. Patients treated with both modalities more often prefer peritoneal dialysis to hemodialysis.
Survival rates on dialysis depend on the underlying disease process. Five-year Kaplan-Meier survival rates vary from 21% for patients with diabetes to 47% for patients with glomerulonephritis. Overall 5-year survival is currently estimated at 36%. Patients undergoing dialysis have an average life expectancy of 3–4 years, but survival for as long as 25 years is seen depending on the disease entity. Studies are conflicting regarding the survival advantage associated with either peritoneal dialysis or hemodialysis.
KIDNEY TRANSPLANTATION
Up to 50% of all patients with ESRD are suitable for transplantation. Age is becoming less of a barrier. Two-thirds of kidney transplants come from deceased donors, with the remainder from living related or unrelated donors. Immunosuppressive drugs include corticosteroids, azathioprine, mycophenolate mofetil, tacrolimus, cyclosporine, and rapamycin. A patient with a deceased-donor renal transplant typically requires stronger immunosuppression than patients with living related kidney donor transplants. However, this depends to a great extent on the degree of HLA-type matching. The 1- and 5-year kidney graft survival rates are approximately 94% and 76%, respectively, for living related and living unrelated donor transplants and 88% and 65%, respectively, for deceased donor transplants. The average wait for a cadaveric transplant is 2–4 years; this is becoming progressively longer as more people are going onto waiting lists while the deceased donor pool is not expanding. Aside from medication use, the life of a transplanted patient can return to nearly normal.
PROGNOSIS
Mortality is higher for patients undergoing dialysis than for age-matched controls. Yearly mortality is 21.2 deaths per 100 patient-years. The expected remaining lifetime for the age group 55–64 is 22 years, whereas that of the ESRD population is 5 years. The most common cause of death is cardiac dysfunction (45%). Other causes include infection (14%), cerebrovascular disease (6%), and malignancy (4%). Diabetes, age, a low serum albumin, lower socioeconomic status, and inadequate dialysis are all significant predictors of mortality.
For those who require dialysis to sustain life but elect not to undergo dialysis, death ensues within days to weeks. In general, uremia develops and patients lose consciousness prior to death. Arrhythmias can occur as a result of electrolyte imbalance. Volume overload and dyspnea can be managed by volume restriction and opioids as described in Palliative Care & Pain Management. Meticulous efforts at palliative care are essential.

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