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Practice of Geriatrics
Robert D. Lindeman, M.D.
Pathophysiology of the Aging Kidney
Evaluation of Renal Function in the Elderly
Renal Diseases in the Elderly
Renal Calculi
Disturbances in Sodium and Water Balance
Disturbances in Potassium Balance
Disturbances in Acid-Base Balance
The accuracy and simplicity with which renal clearance measurements can be performed, requiring only timed urine samples and blood samples drawn at the midpoints of these periods, has made the kidney an ideal organ system for the study of changes that occur with aging. Both cross-sectional and longitudinal studies using mean values suggest that a dramatic decrease in kidney function occurs as one ages. One major problem is the need to distinguish between changes related to “normal” aging and changes influenced by disease. For the purposes of discussion, one can separate medical renal diseases in the elderly by anatomic sites of involvement, etiologic agents, or clinical presentations. Each approach has its advantages and disadvantages.
In this chapter, the last approach is used because it best meets the needs of geriatric clinicians who are faced with clinical challenges that require a problem-solving, differential diagnostic approach. After opening discussions of the pathophysiology of the normal aging kidney and the tests available to evaluate kidney function in the elderly, subsequent sections of the chapter deal with the diagnosis and management of acute renal failure, nephrotic syndrome, chronic renal failure, and stone formation, in that order. Urinary tract infections are discussed in Chapter 38.
This approach involves obvious overlaps. For example, diseases affecting the renal vessels (arteriolar nephrosclerosis, occlusive arterial disease including renal artery stenosis due to atherosclerosis, and vasculitis) most often present as chronic renal insufficiency but can present acutely or with hypertension or hematuria as the principal manifestations. Analgesic abuse can produce both acute and chronic renal failure and is therefore discussed under both headings.
In the normal young adult, the renal capacity to regulate fluid and electrolyte balance far exceeds the ordinary demands for conservation and excretion. Even when this capacity is substantially decreased in old age, renal function still allows adequate regulation of the volume and composition of extracellular fluid. Inability to maintain normal extracellular electrolyte concentrations is generally due to extrarenal defects in the regulatory (homeostatic) mechanisms rather than to insufficient renal function. Nevertheless, the subspecialty of nephrology has traditionally dealt with fluid, electrolyte, and acid-base balances, and because these functions involve a number of problem areas that specifically or predominantly affect the elderly, these will be discussed in this chapter.
Renal function declines after the age of 40 years at a mean rate of 1% per year. These observations, first reported from cross-sectional analyses, were confirmed in a population of normal aging subjects who were followed longitudinally.1 However, when the same subjects were later restudied by calculating regression equations for each individual, it was found that one third of the subjects showed no decline over periods of up to 23 years.2 The decrease in mean creatinine clearance, then, occurred primarily in the other two thirds, who showed decreases in renal function, some very appreciable. There has been a growing awareness, confirmed in functional tests of other organ systems, that a decline in function with age is not inevitable (i.e., there is no progressive involutional process whereby kidney function deteriorates with age). The terms successful and usual aging have been used to distinguish between the values seen in some subjects who weather aging well and the mean values obtained in any “normal” aging population. Much of the decrease in the latter is due to the superimposition of asymptomatic or at least undocumented pathology.
Changes in most renal functions (renal blood flow, tubular secretory and reabsorptive maximums, concentrating and diluting abilities, ability to excrete an acid load, etc.) tend to parallel changes in glomerular filtration rates.3 With age, renal blood flow appears to shift from the cortical to the juxtamedullary nephrons. As cortical glomeruli become obsolete (sclerotic), the vasculature atrophies and disappears. In contrast, as the juxtamedullary glomeruli become obsolete, a shunt forms between the afferent and efferent arterioles so that blood flow is maintained but no glomerular filtrate is generated. The finding that renal blood flow decreases more rapidly than glomerular filtration rate in the elderly appears to be inconsistent with these observations. One possible explanation is that, in the elderly there may be a relative vasoconstriction of the glomerular efferent arteriole as opposed to the afferent arteriole, thereby raising glomerular pressure and filtration. Another potential explanation is that the filtration fraction (glomerular filtration rate/effective renal plasma flow) is higher in the juxtamedullary than in the cortical nephrons, and the elderly lose primarily the latter. Glomerular permeability to albumin, other proteins, and infused substances, such as hemoglobin or dextran, remains unaltered by age.
The most important clinical function that requires monitoring with age is the glomerular filtration rate (GFR). The most reproducible clinical measure of GFR is the creatinine clearance. In a study by Rowe and colleagues1 of the Baltimore Longitudinal Study of Aging population, the mean true creatinine clearance rates fell from 140 mL/minute/1.73 m2 at age 25 to 34 years to 97 mL/minute/1.73 m2 at age 75 to 84 years.1 Nevertheless, the mean serum creatinine concentrations rose insignificantly from 0.81 to 0.84 mg/100 mL. This occurs because creatinine production falls at nearly the same rate as the renal clearance of creatinine, reflecting the decrease in body muscle mass that occurs with age. The practical implication of this observation is that the serum creatinine concentration, when used alone in the older patient, must be interpreted with this change in mind when it is used to determine or modify dosages of drugs cleared totally (e.g., aminoglycoside antibiotics) or partially (e.g., digoxin) by the kidney. Also, drugs that compete with the tubular secretion of creatinine (e.g., trimethoprim-sulfamethoxazole, cimetidine, and cefoxitin) cause an increase in serum creatinine concentration while not changing the true GFR.
The serum urea nitrogen (SUN) and urea clearance similarly make use of endogenously produced urea as the test substance. Since large amounts of urea may be reabsorbed in the tubule at low flow rates, vigorous hydration must be used to make the clearance results interpretable. Dietary protein intake also affects results appreciably. Therefore, in general, creatinine determinations have largely replaced urea and urea nitrogens in the evaluation of renal function.
A formula derived by Cockcroft and Gault4 can be used to predict creatinine clearances from serum creatinine concentrations using age and weight for men as follows:

For females, this value is multiplied times 0.85. This formula has been shown to be unreliable in very old patients, however.
Generally, tests of tubular function add little to one’s knowledge of renal functional pathology. Although the response to 12 or more hours of water deprivation can be determined in terms of ability to concentrate the urine, this test creates some risk for older patients by imposing on them a period of dehydration sufficient to expose the kidneys in patients with underlying renal disease to further damage. Most normal older adults should be able to increase urine osmolality to 800 to 900 mOsm/kg H2O (specific gravity 1.020 to 1.022). Failure to increase urine osmolality much above 300 mOsm/kg H2O (specific gravity 1.010) implies tubular disease, diabetes insipidus, obstructive uropathy, or advanced renal disease.
Renal disease may present with asymptomatic urinary abnormalities identified with screening urinalysis. Hematuria can be due to renal parenchymal disease, diseases of the collecting systems, or systemic coagulation defects. The presence of red cell casts in a freshly voided urine is consistent only with a glomerular cause. The finding of associated proteinuria or an elevated serum creatinine concentration also suggests renal parenchymal disease.
If the lower urinary tract is thought to be the source of hematuria, a segmental analysis of a voided urine specimen may be helpful. Initial hematuria suggests a urethral source, terminal hematuria suggests a bladder source, and constant hematuria suggests a source in the upper urinary tract. Evaluation of isolated hematuria should include a urine culture, radiologic evaluation (intravenous pyelography [IVP] or sonography) to rule out renal parenchymal masses, and a urologic consultation for cystoscopy. In addition, a platelet count, bleeding time, prothrombin time, and partial thromboplastin time should be obtained to rule out a coagulopathy. In approximately 85% of patients, a cause of bleeding can be found on work-up, with malignancies, most often bladder, hypernephroma, and prostate tumors, accounting for one third of the cases of hematuria.
Normal protein excretion in the elderly does not differ significantly from that in young adults. Significant proteinuria is defined as greater than 150 mg urinary protein excretion per 24 hours. The dipstick is a good screening method for the detection of proteinuria but detects only albumin; light chains, which are present in patients with multiple myeloma, and low-molecular-weight protein (tubular protein) must be detected with the sulfosalicylic acid test. When the proteins excreted in the urine are primarily albumin and higher molecular weight proteins, the pathology is believed to be glomerular in origin. Generally a level of 3 g protein a day is used to separate nephrotic proteinuria from non-nephrotic proteinuria. On microscopic examination of the urine, the finding of pyuria, hematuria, and casts is of some value in determining the cause of the renal disease in the elderly, as it is in younger patients.
A variety of imaging techniques are available to evaluate the genitourinary system in the elderly. Ultrasonography is a noninvasive and safe test that can provide many diagnostic clues, showing kidney size, hydronephrosis, and solid or cystic parenchymal renal masses. Preceding a renal biopsy, an ultrasound examination should be performed to ensure the presence of two normal sized kidneys. An IVP will demonstrate sites of obstruction and other pathology (e.g., papillary necrosis). Elderly patients are placed at risk when undergoing dehydration and thereby can develop contrast media–induced acute renal failure, especially when there is an underlying diagnosis of diabetes mellitus, renal insufficiency, hypertension, or, especially, multiple myeloma.
Computed tomographic (CT) scans, angiography, and magnetic resonance imaging (MRI) are additional procedures available for the evaluation of renal masses, unexplained hematuria, or obstruction. Finally, for patients with suspected primary glomerular disease or unexplained renal failure, a renal biopsy may be indicated after all other available means of establishing a diagnosis have been exhausted.
The most common presenting manifestations of renal disease in the elderly, as in younger persons, are acute and chronic renal insufficiency (azotemia), proteinuria (nephrotic and non-nephrotic), and hematuria. Often the definitive diagnostic test is the renal biopsy. Moorthy and Zimmerman5 reviewed the clinical indications and histologic diagnoses in 115 patients, aged 60 years or more, who underwent renal biopsy. The major clinical presentations were renal insufficiency in 57 patients, nephrotic syndrome in 35 patients, and hematuria with variable amounts of proteinuria in 23 patients. Rapidly progressive (crescentic) glomerulonephritis (19 patients) was the most common cause of renal insufficiency. Membranous glomerulopathy and minimal change lesions were the most commonly observed causes of nephrotic syndrome.
One of the largest series of biopsy (449 cases) and autopsy (51 cases) studies of renal disease in the elderly is that reported from the Armed Forces Institute of Pathology, which reviewed pathologic diagnoses in 500 patients over the age of 60 years (Table 49-1).6 Although it must be recognized that this study is not an accurate reflection of the true prevalence of renal disease in the elderly because biopsy in diabetics and hypertensives with renal insufficiency often is not done, it does show that the spectrum of renal diseases seen in the elderly is no different from that seen in younger persons; only the frequencies are different.


Acute Renal Failure
In two large European series,7,8 35% of patients with acute renal failure (ARF) were older than 65 and 70 years, respectively. One of these studies8 indicated that the incidence of ARF was three times more frequent than expected in the elderly (age over 70 years). In another study in which acute glomerulonephritis and acute interstitial nephritis were excluded as causes of ARF, 64% of patients were older than 60 years and 36% were older than 70 years.9
Elderly patients have the same spectrum of causes of ARF as younger patients. However, within that spectrum there are some significant differences in the incidence of some causes in the elderly as opposed to the young. Obstructive disease, renal embolization or thrombosis, and hypovolemic postischemic acute tubular necrosis (ATN) were more common causes of ARF in the elderly; acute glomerulonephritis and pigment-induced (myoglobinuric) ATN were more common causes in the young. ARF can be divided into three major categories—specifically, prerenal, renal, and postrenal. The serum urea nitrogen to serum creatinine ratios of prerenal and postrenal ARF tend to run more than 20 to 1, whereas the ratio in renal disease–associated ARF tends to average 10 to 14 to 1 depending on dietary protein intake.
Prerenal ARF is due to renal hypoperfusion (dehydration, congestive heart failure, sepsis) and is often associated with recovery of renal function after correction of the hemodynamic disturbance. It can also occur in patients with excessive protein catabolism (intestinal bleeding, hematoma). Many milder forms of prerenal ARF remain undetected because they are treated with rehydration or with treatment for congestive heart failure or sepsis. Lamiere and associates7 required a serum creatinine level of 3 mg/100 mL or more before a diagnosis of ARF could be made. In one study in which records of all patients admitted to three acute care geriatric units in England were reviewed, more than half of those with increased urea or creatinine concentrations had prerenal ARF.10
The kidney is very sensitive to the action of toxic agents because it receives 25% of the resting cardiac output. It also has a very high capacity for concentrating solutes, so the medullary portion of the kidney is exposed to high concentrations of these toxic compounds. The elderly, because of their age-related, compromised renal function and their use of many prescribed and over-the-counter drugs, are more susceptible to toxic renal injury than the young.
The use of nonsteroidal anti-inflammatory agents (NSAIDs) or angiotensin-converting enzyme (ACE) inhibitors in the elderly is largely responsible for the increasing incidence of iatrogenic hemodynamically mediated ARF in the elderly. The use of NSAIDs increases with age, but renal function impairment increases disproportionately. A number of clinical conditions (e.g., congestive heart failure, decompensated cirrhosis, nephrotic syndrome, and chronic renal failure) require local synthesis of vasodilating prostaglandins to maintain renal perfusion. Introduction of these drugs allows unopposed vasoconstriction to occur, resulting in an acute ischemic renal insult. Other risk factors for NSAID- and ACE inhibitor–induced ARF include underlying renal disease with or without renal insufficiency, hypertension, diabetes mellitus, diuretic therapy, volume depletion, and atherosclerotic cardiovascular disease.
Patients with bilateral renal artery stenosis or severe chronic heart failure may develop ARF when ACE inhibitors are prescribed. In fact, it is not uncommon for physicians to detect bilateral atheromatous renal artery disease in patients with impaired renal function because of an acute deterioration of condition after therapy with ACE inhibitors for hypertension or congestive heart failure is started.
Postischemic acute tubular necrosis (ATN) is the most common type of ATN and is relatively more frequent in the elderly than in younger individuals. Renal hypoperfusion can result from a variety of insults, the most common being septic shock, hypovolemia, hepatobiliary or pancreatic disease, and cardiovascular catastrophes. Many cases start as prerenal ARF that is recognized too late or not at all. Generally, renal hypoperfusion is due to systemic hypotension in a situation in which autoregulatory capacities for preservation of renal blood flow and GFR are either overwhelmed or are interrupted by preexisting renal (vascular) disease or by therapeutic interventions.
The diagnosis of hypovolemia in the elderly is often difficult. There is no reliable laboratory test that can make this diagnosis because vital signs or orthostatic decreases in blood pressure and increases in pulse rate and changes in body weight can be difficult to evaluate. The differentiation between prerenal (often hypovolemic) ARF and established renal ARF (ATN) depends on the analysis of urinary electrolytes and osmolality. The fractional excretion of sodium (FEna), however, is not very reliable in elderly patients.
Antibiotics, especially the aminoglycosides, are the predominant causes of nephrotoxic ATN. The monitoring of serum concentrations of the aminoglycosides has greatly reduced the incidence of ARF due to this cause, but even with careful monitoring some cases still occur. The radiocontrast agents now used in IVP, angiography, and computed tomography are the second most common cause of drug-induced ATN. The principal contrast agents currently in use are the sodium and meglumine salts of diatrizoate, iothalamate, metrizamide, and ioxadate. The incidence of contrast-induced ARF is less than 2% unless risk factors exist, and most cases of ARF from this cause are reversible. Acute renal failure following oral cholecystography or biliary tract visualization with the use of iopanoic acid (Telepaque) is now rare unless excessively high doses are used. Factors that increase risk include age, diabetes mellitus, preexisting renal insufficiency, multiple myeloma, renal hypoperfusion (dehydration), hypertension, and hepatic disease. The risk of contrast-induced ARF in the elderly diabetic with preexisting renal insufficiency approaches 100%, and much of this may be irreversible. Other causes of ATN in the elderly population include heavy metal exposure, cisplatinum therapy, hemoglobinuria, myoglobinuria, and exposure to fluorinated anesthetic agents (Penthrane).
Drug-induced acute interstitial nephritis (AIN) has become an increasingly common cause of ARF; AIN may also be seen as a complication of infectious or systemic disease. More than 40 drugs have been implicated as possible etiologic agents, with the penicillins (penicillin G, methicillin, ampicillin, oxacillin, nafcillin), cephalosporins, and NSAIDs being most commonly involved. Methicillin is the most frequently reported penicillin causing ARF; at times nearly 20% of patients treated with this drug develop ARF, perhaps because higher doses are used over a long period in patients with staphylococcal septicemia and endocarditis. Patients with penicillin-associated AIN frequently develop fever, rash, and eosinophilia or eosinophiluria in addition to a nonoliguric progressive azotemia.
The widespread use of NSAIDs has led to many reports of acute to chronic renal failure, especially in the elderly. Patients taking NSAIDs who present with ARF and nephrotic syndrome often have a histologic picture showing a combination of AIN and minimal change disease.
Although acute glomerulonephritis (AGN) is generally regarded as a disease of children and young adults, a number of reports in the literature indicate that AGN in the elderly is more common than is generally believed.11 The essential clinical features (hematuria, proteinuria, sodium and fluid retention, decreased renal function, and hypertension) are no different in the elderly. The diagnosis may be obscured by the presence of preexisting conditions or preconceived ideas about its occurrence in the elderly. Adults frequently have a picture of cardiovascular decompensation that is attributed to underlying atherosclerotic or hypertensive heart disease, and azotemia that is either overlooked or attributed to prerenal causes. The diagnostic red cell casts are often not sought because of a low index of suspicion. Although histologic examination in many of these patients shows a poststreptococcal or postinfectious acute proliferative glomerulonephritis, it may be difficult to distinguish these patients clinically from patients with rapidly progressive (crescentic) glomerulonephritis or glomerulonephritis resulting from a systemic disease (systemic lupus erythematosus, vasculitis, subacute bacterial endocarditis, Henoch-SchÖnlein’s purpura).
Postrenal obstruction is an important cause of ARF because it is common and is often treatable. Prostatic hyperplasia is the most frequent cause. Hospitalized elderly patients on bed rest may be unable to generate the necessary pressure to void if they cannot stand. The frequent use of anticholinergic drugs, particularly the tricyclic antidepressants, may potentiate urinary retention.
The first step in management of patients with acute renal failure is to identify and correct any prerenal or postrenal component. Prerenal azotemia should be suspected whenever the SUN–serum creatinine ratio exceeds 20 to 1, the urine osmolality exceeds 500 mOsm/kg H2O, the urinary sodium concentration falls below 20 mEq/liter and/or the fractional excretion of sodium (FEna) is less than 1% (this last measurement is the percentage of filtered sodium excreted in the urine). If a diagnosis of prerenal azotemia is made, volume should be replaced with saline, blood, or blood products. If cardiac output is impaired, the patient should be treated with a combination of diuretics, nitrates, inotropic agents (digoxin), and/or afterload-reducing agents (ACE inhibitors) to maximize cardiac output.
Postrenal factors, again if the SUN–serum creatinine ratio exceeds 20 to 1, should be suspected and evaluated by bladder catheterization, renal ultrasound, or nuclide urography. If an obstruction is documented and cannot be relieved by catheterization, cystoscopy with stent placement or percutaneous nephrostomy may be indicated.
Subsequent treatment should focus on maintaining control of uremic symptoms by dialysis and dietary protein restriction (caloric intake must be maintained), maintaining fluid, electrolyte, and acid-base balance, and avoiding and controlling any possible infectious complications. Hemodialysis or peritoneal dialysis should be selected based on institutional capabilities, access availability, and contraindications (e.g., heparinization).
Nephrotic Syndrome
The nephrotic syndrome consists of the urinary excretion of more than 3 g protein per day with other features that are a consequence of this continued protein loss (hypoalbuminemia, hyperlipidemia, edema, and a hypercoagulable state). Hypertension and renal failure are seen in about a third of the patients. The nephrotic syndrome can result from primary glomerular disease or from glomerular disease resulting from exposure to drugs, allergens, infection, neoplastic disease, or multisystem disease. The incidence of nephrotic syndrome is at least as common in the elderly as it is in younger age groups.
Brown11 reviewed the histopathologic findings in five series with 215 patients over the age of 60 years who presented with nephrotic syndrome. Histopathologic examination showed membranous nephropathy in 38%, minimal change nephropathy in 18%, proliferative glomerulonephritis in 13%, amyloidosis in 15%, and a variety of other lesions in the remaining 17%. The incidence of membranous nephropathy and amyloidosis was higher than it is in younger adults, that of proliferative glomerulonephritis was much lower, and the incidence of minimal change disease was comparable but much lower than it is in children. A subsequent study12 showed a similar incidence of primary glomerular diseases in individuals older than 60 years compared to young adults, but there was a different distribution of causes. IgA nephritis was seen less frequently, and membranous glomerulopathy and pauci-immune crescentic glomerulonephritis were more frequent. Glomerulopathies resulting from systemic disease are more common in the elderly because there is an increased incidence of such underlying diseases as diabetes mellitus, amyloidosis (dysproteinemias), neoplastic disease, vasculitis, and scleroderma in older people.
Membranous nephropathy (MN) is consistently the most common cause of nephrotic syndrome in the elderly; at least 85% of patients with MN present with nephrotic proteinuria. The two most common causes of secondary MN are drugs (e.g., NSAIDs) and cancer. Brown11 reported that 11% of patients with MN had an underlying malignancy.
It remains unclear whether the prognosis of elderly patients with MN is worse than that of younger persons; however, it does appear that older patients are more susceptible to the extrarenal complications of the nephrotic syndrome and its treatment (e.g., cardiovascular, thrombotic, and infectious events).13 Corticosteroid therapy alone appears to be of little benefit in inducing remission or preventing deterioration of renal function; the combination of an immunosuppressive (e.g., chlorambucil and corticosteroids) appears more likely to be helpful, but side effects of treatment are frequent.
The clinical presentation of minimal change nephropathy (MCN) is similar in old and young (i.e., nephrotic syndrome), but older individuals are much more likely to have nonselective proteinuria, microscopic hematuria, hypertension, and renal insufficiency. While Lorca and Ponticelli,13 in reviewing 11 series, reported that 80% of patients with MCN responded initially to treatment with corticosteroids or cytotoxic agents, almost a third experienced a relapse, and half then developed renal failure or died. These authors recommended treating the patient initially with corticosteroids followed by a cytotoxic agent in 12 weeks if steroids are not tolerated or are not effective.
In patients with sclerotic lesions the presence of nephrotic syndrome and the finding of fusion of foot processes on electron microscopy are the most reliable features for a diagnosis of idiopathic focal and segmental glomerulosclerosis. Although some of these patients will respond to prolonged administration of corticosteroid or cytotoxic agents, the risk of side effects generally outweighs the benefits of these agents in the elderly.
Rapidly progressive glomerulonephritis (RPGN) is the result of a number of diseases of immunologic pathogenesis resulting in a renal lesion characterized by extracapillary proliferation in the glomeruli (crescent formation within Bowman’s capsule). These patients often test positive for serum p-antinuclear cytoplasmic antibody (p-ANCA). Keller and colleagues14 reported a linear increase in the incidence of RPGN with age; over 40% of their patients were older than 60 years. Although they used aggressive corticosteroid-immunosuppressive therapy in their elderly patients and noted better results in maintenance of self-sustaining renal function in treated versus untreated patients, they found that the long-term efficacy of such treatment was limited and the complication rate was high. Initial oliguria was the most significant risk factor for permanent loss of renal function.
Nephritis associated with systemic lupus erythematosus (SLE) can be classified into one of four histologic patterns—mesangial, focal proliferative, diffuse proliferative, or membranous. The diagnosis is established by a positive antinuclear antibody (ANA) titer in the serum or, more specifically, by positive results on the antideoxyribonucleoprotein antibody (anti-DNA) test. Renal involvement appears to be less common in the elderly than in younger populations. The prognosis is determined by both renal and extrarenal involvement. Impressive responses have been reported with either azathioprine or cyclophosphamide combined with prednisone therapy.
Diabetic nephropathy is the most frequent cause of glomerular disease associated with systemic illness in the elderly. The diagnosis can be made clinically from a history of long-standing diabetes, evidence of proteinuria (usually in the nephrotic range), diabetic retinopathy, and hypertension. Once nephrotic proteinuria develops, the disease follows a downhill course (3 to 5 years) ending in dialysis regardless of treatment. Control of blood pressure is important in slowing the rate of deterioration of renal function. The use of ACE inhibitors or angiotensin-II receptor blockade even in normotensive individuals to promote efferent arteriolar vasodilatation and a decrease in glomerular capillary pressure also slows the rate of deterioration of renal function. Tight control of blood glucose, in contrast, does not appear to affect the course of the disease. Vigorous treatment of urinary tract infections and avoidance of analgesics to prevent the development of papillary necrosis are warranted.
Amyloidosis is characterized by deposition of amyloid fibrils in glomerular capillary loops. In primary amyloidosis, these fibrils are light chains that have a composition similar to those of Bence Jones proteins. Patients with plasma cell dyscrasias often have an amyloidosis similar to that seen with primary amyloidosis. Secondary amyloidosis is associated with such chronic inflammatory diseases as rheumatoid arthritis, tuberculosis, chronic bone, lung, or urinary tract infections, and inflammatory bowel disease. The amyloid fibrils, in contrast, are composed of a nonimmunoglobulin protein and are distributed throughout the organ systems in a different pattern from that seen in primary amyloidosis. All nephrotics over the age of 50 years should undergo performance of urine and serum electrophoresis because amyloidosis is a frequent cause of secondary nephrotic syndrome.
Lesions associated with the collagen vascular diseases (e.g., SLE, vasculitis, and Wegener’s granulomatosis) respond well to corticosteroid or cytotoxic or immunosuppressant therapy, whereas most other lesions tend to be resistant to treatment. Because of the potential adverse effects of these treatments, renal biopsy is important in determining whether or not therapeutic trials should be initiated in patients in whom the diagnosis is unclear.
Chronic Renal Failure
Chronic renal failure results from irreversible damage to both kidneys from a wide variety of causes. Up to 90% of kidney function may be lost without significant morbidity. The physician’s role in these patients is to prevent progression of the renal lesions and worsening of the condition by managing hypertension, infection, obstructive uropathy, heart failure, and dehydration. Some of the more common clinical entities that can cause chronic renal failure without preceding nephrotic syndrome are discussed in the following section.
Occlusive arterial disease can cause either acute or chronic renal failure. Renal arterial embolization or thrombosis may occur in patients with acute myocardial infarction, chronic atrial fibrillation, and subacute bacterial endocarditis. Symptoms vary from essentially a slowly progressive, clinically silent event to acute severe flank pain and tenderness, hematuria, hypertension, and fever. Intravenous pyelography or renal scans followed by aortography are used to establish a diagnosis. Anticoagulant therapy may be beneficial; surgery is generally not indicated for embolization but may be helpful in selected patients with renal arterial arteriosclerosis or when an intra-abdominal aortic aneurysm is the underlying cause.



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