eMedicine Specialties > Nephrology > Glomerular Diseases

Glomerulonephritis, Chronic

Moro O Salifu, MD, MPH, FACP, Associate Professor, Department of Internal Medicine, Chief, Division of Nephrology, Director of Nephrology Fellowship Program and Transplant Nephrology, State University of New York Downstate Medical Center
Barbara G Delano, MD, MPH, Director of Home Hemodialysis and Peritoneal Dialysis, Professor, Department of Internal Medicine, Division of Nephrology, State University of New York at Brooklyn

Updated: Oct 23, 2009

Introduction

Background

Nearly all forms of acute glomerulonephritis have a tendency to progress to chronic glomerulonephritis. The condition is characterized by irreversible and progressive glomerular and tubulointerstitial fibrosis, ultimately leading to a reduction in the glomerular filtration rate (GFR) and retention of uremic toxins. If disease progression is not halted with therapy, the net result is chronic kidney disease (CKD), end-stage renal disease (ESRD), and cardiovascular disease. The diagnosis of CKD can be made without knowledge of the specific cause.

The National Kidney Foundation defines CKD as (1) evidence of kidney damage based on abnormal urinalysis results (eg, proteinuria, hematuria) or structural abnormalities observed on ultrasound images or (2) a GFR of less than 60 mL/min for 3 or more months. Based on this definition, the National Kidney Foundation developed guidelines that classify the progression of renal disease into 5 stages, from kidney disease with a preserved GFR to end-stage kidney failure. This classification includes treatment strategies for each progressive level, as follows:

• Stage 1: This stage is characterized by kidney damage with a normal GFR (>90 mL/min). The action plan is diagnosis and treatment, treatment of comorbid conditions, slowing of the progressing of kidney disease, and reduction of cardiovascular disease risks.
• Stage 2: This stage is characterized by kidney damage with a mild decrease in the GFR (60-90 mL/min). The action plan is estimation of the progression of kidney disease.
• Stage 3: This stage is characterized by a moderately decreased GFR (30-59 mL/min). The action plan is evaluation and treatment of complications.
• Stage 4: This stage is characterized by a severe decrease in the GFR (15-29 mL/min). The action plan is preparation for renal replacement therapy.
• Stage 5: This stage is characterized by kidney failure. The action plan is kidney replacement if the patient is uremic.

At the later stages of glomerular injury, biopsy results cannot help distinguish the primary disease. Histology and clues to the etiology are often derived from other systemic diseases, if present. Considerable cause-specific variability is observed in the rate at which acute glomerulonephritis progresses to chronic glomerulonephritis.

Pathophysiology

Reduction in nephron mass from the initial injury reduces the GFR. This reduction leads to hypertrophy and hyperfiltration of the remaining nephrons and to the initiation of intraglomerular hypertension. These changes occur in order to increase the GFR of the remaining nephrons, thus minimizing the functional consequences of nephron loss. The changes, however, are ultimately detrimental because they lead to glomerulosclerosis and further nephron loss.

In early renal disease (stages 1-3), a substantial decline in the GFR may lead to only slight increases in serum creatinine levels. Azotemia (ie, a rise in BUN and serum creatinine levels) is apparent when the GFR decreases to less than 60-70 mL/min. In addition to a rise in BUN and creatinine levels, the substantial reduction in the GFR results in decreased production of (1) erythropoietin, thus resulting in anemia; (2) decreased production of vitamin D, resulting in hypocalcemia, secondary hyperparathyroidism, hyperphosphatemia, and renal osteodystrophy; (3) reduction in acid, potassium, salt, and water excretion, resulting in acidosis, hyperkalemia, hypertension, and edema; and (4) platelet dysfunction, leading to increased bleeding tendencies.

Accumulation of toxic waste products (uremic toxins) affects virtually all organ systems. Azotemia occurring with the signs and symptoms listed above is known as uremia. Uremia occurs at a GFR of approximately 10 mL/min. Some of these toxins (eg, BUN, creatinine, phenols, guanidines) have been identified, but none has been found to be responsible for all the symptoms.

Frequency

United States

Chronic glomerulonephritis is the third leading cause of ESRD and accounts for 10% of patients on dialysis in the United States.

International

Chronic glomerulonephritis accounted for up to 40% of patients on dialysis in Japan and some Asian countries. However, more recent data suggest that, in Japan for instance, the rate of chronic glomerulonephritis in patients on dialysis is 28%. The cause of this declining rate is not known. Concurrent with the decline in chronic glomerulonephritis in these countries is an increase in diabetic nephropathy in up to 40% of patients on dialysis.

Mortality/Morbidity

ESRD and death are common outcomes unless renal replacement therapy is instituted.

Clinical

History

The history should focus on cause-specific symptoms to determine the causes of CKD (if unknown) and on symptoms related to uremia to determine if renal replacement therapy is needed.

• Cause-specific history: Obtain a cause-specific history so that further workup and management of the disease (if systemic) can be planned.
• Uremia-specific history
  • The following symptoms suggest uremia:
    • Weakness and fatigue
    • Loss of energy, appetite, and weight
    • Pruritus
    • Early morning nausea and vomiting
    • Change in taste sensation
    • Reversal in sleep pattern (ie, sleepiness in daytime, wakefulness at night)
    • Peripheral neuropathy
    • Seizures
    • Tremors
  • The presence of edema and hypertension suggests volume retention.
  • Dyspnea or chest pain that varies with position suggests fluid overload and pericarditis, respectively.
  • Leg cramps may suggest hypocalcemia or other electrolyte abnormalities.
  • Weakness, lethargy, and fatigue may be due to anemia.

Physical

Cause-specific physical examination findings are discussed in articles on the specific causes. See Causes for links to such articles.

• Uremia-specific findings
  • Hypertension
  • Jugular venous distension (if severe volume overload is present)
  • Pulmonary rales (if pulmonary edema is present)
  • Pericardial friction rub in pericarditis
  • Tenderness in the epigastric region or blood in the stool (possible indicators for uremic gastritis or enteropathy)
  • Decreased sensation and asterixis (indicators for advanced uremia)

Causes

The progression from acute glomerulonephritis to chronic glomerulonephritis is variable. Whereas complete recovery of renal function is the rule for patients with poststreptococcal glomerulonephritis, several other glomerulonephritides, such as immunoglobulin A (IgA) nephropathy, often have a relatively benign course and many do not progress to ESRD.

• Rapidly progressive glomerulonephritis or crescentic glomerulonephritis: Approximately 90% of patients progress to ESRD within weeks or months.
• Focal segmental glomerulosclerosis: Approximately 80% of patients progress to ESRD in 10 years. Patients with the collapsing variant, which is termed malignant focal segmental glomerulosclerosis, have a more rapid progression. This form may be idiopathic or related to HIV infection.
• Membranous nephropathy: Approximately 20-30% of patients with membranous nephropathy progress to chronic renal failure (CRF) and ESRD in 10 years.
• Membranoproliferative glomerulonephritis: Approximately 40% of patients with membranoproliferative glomerulonephritis progress to CRF and ESRD in 10 years.
• IgA nephropathy: Approximately 10% of patients with IgA nephropathy progress to CRF and ESRD in 10 years.¹
• Poststreptococcal glomerulonephritis: Approximately 1-2% of patients with poststreptococcal glomerulonephritis progress to CRF and ESRD. Older children who present with crescentic glomerulonephritis are at greatest risk.
• Lupus nephritis: Overall, approximately 20% of patients with lupus nephritis progress to CRF and ESRD in 10 years; however, patients with certain histologic variants (eg, class IV) may have a more rapid decline..

Differential Diagnoses

Other Problems to Be Considered

Mesangial glomerulonephritis

Workup

Laboratory Studies

• Urinalysis
  • The presence of dysmorphic RBCs, albumin, or RBC casts suggests glomerulonephritis as the cause of renal failure.
  • Waxy or broad casts are observed in all forms of CKD, including chronic glomerulonephritis.
  • Low urine-specific gravity indicates loss of tubular concentrating ability, an early finding in persons with CDK.
• Urinary protein excretion
  • This can be estimated by calculating the protein-to-creatinine ratio on a spot morning urine sample. The ratio of urinary protein concentration (in mg/dL) to urinary creatinine (in mg/dL) reflects 24-hour protein excretion in grams. For instance, if the spot urine protein value is 300 mg/dL and the creatinine value is 150 mg/dL, then the ratio is 300 divided by 150, which equals 2. Thus, in this example, the 24-hour urine protein excretion is 2 g.
  • The estimated creatinine clearance rate is used to assess and monitor the GFR. The 2 formulas available to calculate the value are the Cockroft-Gault formula, which estimates creatinine clearance, and the Modification of Diet in Renal Disease Study (MDRD) formula, which is used to calculate the GFR. The Cockroft-Gault formula is simple to use but overestimates the GFR by 10-15% because creatinine is both filtered and secreted. The MDRD formula is much more complex but is available as a PDA through the National Kidney Foundation or can be calculated online through the Hypertension, Dialysis, and Clinical Nephrology Web site.
  • The estimated creatinine clearance rate is also used to monitor response to therapy and to initiate an early transition to renal replacement therapy (eg, dialysis access placement, transplantation evaluation). The degree of proteinuria, especially albuminuria, helps predict renal prognosis in patients with chronic glomerulonephritis. Patients with greater than 1 g/d have an increased risk of progression to ESRD.
    
    In a study of 38 patients with chronic glomerulonephritis, Hayakawa et al examined the relationship between plasma adiponectin, leptin, and proteinuria levels; glomerular filtration rate; and metabolic risk factors.² They found that plasma adiponectin levels were much higher in patients with heavy proteinuria (38.8 +/- 27.8 μ g/mL) than they were in patients who had mild (13.3 +/- 5.1 μ g/mL, P <0.001) or moderate proteinuria (18.1 +/- 8.0 μ g/mL, P <0.01). Serum leptin levels, however, did not differ according to the degree of proteinuria.
• CBC count
  • Anemia is a significant finding in patients with some decline in the GFR.
  • Physicians must be aware that anemia can occur even in patients with serum creatinine levels of less than 2 mg/dL. Even severe anemia can occur at low serum creatinine levels. Anemia is the result of marked impairment of erythropoietin production.
• Serum chemistry
  • Serum creatinine and urea nitrogen levels are elevated.
  • Impaired excretion of potassium, free water, and acid results in hyperkalemia, hyponatremia, and low serum bicarbonate levels, respectively.
  • Impaired vitamin D-3 production results in hypocalcemia, hyperphosphatemia, and high levels of parathyroid hormone.
  • Low serum albumin levels may be present if uremia interferes with nutrition or if the patient is nephrotic.

Imaging Studies

• Renal ultrasonogram
  
  
  • Obtain a renal ultrasonogram to determine renal size, to assess for the presence of both kidneys, and to exclude structural lesions that may be responsible for azotemia.
  • Small kidneys often indicate an irreversible process.

Procedures

• Kidney biopsy
  • If the kidney is small, kidney biopsy is usually unnecessary; no specific pattern of disease can be discerned at this point.
  • A kidney biopsy may be considered in the minority of patients who exhibit an acute exacerbation of their chronic disease. This may be particularly pertinent to patients with preserved kidney size and in those with lupus nephritis.

Histologic Findings

In early stages, the glomeruli may still show some evidence of the primary disease.

Treatment

Medical Care

Progression from CKD to ESRD can be slowed by a variety of measures, including aggressive control of diabetes, hypertension, and proteinuria. Dietary protein restriction, phosphate restriction, and hyperlipidemia control may have significant impact on retarding disease progression. Specific therapies for some glomerular diseases (eg, lupus) should be implemented in appropriate settings. Aggressively manage anemia and renal osteodystrophy (eg, hyperphosphatemia, hypocalcemia, hyperparathyroidism) before renal replacement therapy. Also, aggressively manage comorbid conditions, such as heart disease and diabetes.

• The target pressure for patients with proteinuria greater than 1 g/d is less than 125/75 mm Hg; for patients with proteinuria less than 1 g/d, the target pressure is less than 130/80 mm Hg.
  • Angiotensin-converting enzyme inhibitors (ACEIs) are commonly used and are usually the first choice for treatment of hypertension in patients with CRF. ACEIs are renoprotective agents that have additional benefits beyond lowering pressure. ACEIs effectively reduce proteinuria, in part by reducing the efferent arteriolar vascular tone, thereby decreasing intraglomerular hypertension. Particularly, ACEIs have been shown to be superior to conventional therapy in slowing the decline of the GFR in patients with diabetic and nondiabetic proteinuric nephropathies. Therefore, consider ACEIs for treatment of even normotensive patients with significant proteinuria.³
  • The role of angiotensin II receptor blockers (ARBs) in renal protection is increasingly being established, and these medications have been found to retard the progression of CKD in patients with diabetic or nondiabetic nephropathy in a manner similar to that of ACEIs.
  • Combination therapy with ACEIs and ARBs has been shown to confer superior pressure control and preservation of renal function than either therapy alone. Therefore, in patients without hyperkalemia or an acute rise in serum creatinine levels following the use of either therapy, combination therapy should be attempted.
  • Diuretics are often required because of decreased free-water clearance, and high doses may be required to control edema and hypertension when the GFR falls to less than 25 mL/min. Diuretics are also useful in counteracting the hyperkalemic potential of ACEIs and ARBs. However, diuretics should be used with caution when given together with ACEIs or ARBs because the decline in intraglomerular pressure induced by ACEIs or ARBs may be exacerbated by volume depletion induced by diuretics, potentially precipitating acute renal failure.
  • Beta-blockers, calcium channel blockers, central alpha-2 agonists (eg, clonidine), alpha-1 antagonists, and direct vasodilators (eg, minoxidil, nitrates) may be used to achieve the target pressure.
• Because progressive fibrosis is the hallmark of chronic glomerulonephritis, some investigators have focused their work on finding inhibitors of fibrosis in an attempt to slow progression. Of many compounds, pirfenidone, an inhibitor of transforming growth factor beta, and hence of collagen synthesis, has emerged as the candidate compound. Cho et al performed an open label study on 21 patients with idiopathic and postadaptive focal segmental glomerulosclerosis.⁴ They found a median 25% improvement in the rate of decline of the estimated GFR (P <0.01). Pirfenidone did not effect proteinuria or blood pressure. Among the adverse events attributed to therapy were dyspepsia, sedation, and photosensitive dermatitis. Pirfenidone offers hope in slowing progressive fibrosis; however more studies are needed.
• Renal osteodystrophy can be managed early by replacing vitamin D and by administering phosphate binders. Seek and treat nonuremic causes of anemia, such as iron deficiency, before instituting therapy with erythropoietin.
• Discuss options for renal replacement therapy (eg, hemodialysis, peritoneal dialysis, renal transplantation). Arrange permanent vascular access when the GFR decreases to less than 20-25 mL/min, when the serum creatinine level is greater than 4 mg/dL, or if the rate of rise in the serum creatinine level indicates the need for dialysis within 1 year. Arteriovenous fistulas are preferred to arteriovenous grafts because of their long-term high-patency rates and should be placed whenever possible. Place peritoneal dialysis catheters 2-3 weeks prior to anticipated dialysis therapy.
• Treat hyperlipidemia (if present) to reduce overall cardiovascular comorbidity, even though evidence for renal protection is lacking.
• Expose patients to educational programs for early rehabilitation from dialysis or transplantation.

Surgical Care

Create access for dialysis when the GFR decreases to less than 25 mL/min.

Consultations

• Nephrologists: Early referral of patients with CRF to a nephrologist is important for the management of complications and the organization of the transition to renal replacement therapy (eg, hemodialysis, peritoneal dialysis, renal transplantation). Some evidence indicates that early referral of a patient with CRF (serum creatinine, 1.5-2 mg/dL) to a nephrologist improves the short-term outcome.
• Surgeons: When dialysis is imminent, seek consultation for creation of an arteriovenous fistula or graft for the insertion of a peritoneal dialysis catheter.
• Transplantation surgeons: Seek consultations for evaluation for kidney transplantation.

Diet

• Protein-restricted diets (0.4-0.6 g/kg/d) are controversial but may be beneficial in slowing the decline in the GFR and in reducing hyperphosphatemia (serum phosphate, >5.5 mg/dL) in patients with serum creatinine levels of greater than 4 mg/dL. Monitor these patients for signs of malnutrition, which may contraindicate protein restriction.
• Educate patients about how diets rich in potassium help control hyperkalemia.
• Many dietary restrictions are no longer necessary with the initiation of renal replacement therapy.

Activity

• Encourage patients to increase their activity level as tolerated. Increased activity may aid in blood pressure control.

Medication

The goals of pharmacotherapy are to reduce morbidity and to prevent complications.

Angiotensin-converting enzyme inhibitors

For renoprotection. Decrease intraglomerular pressure and, consequently, glomerular protein filtration, by decreasing efferent arteriolar constriction.³

Enalapril (Vasotec)

Competitive inhibitor of ACE. Reduces angiotensin II levels, thus decreases aldosterone secretion. Decreases intraglomerular pressure and glomerular protein filtration by decreasing efferent arteriolar constriction.

Dosing

Adult

2.5-10 mg PO qd; not to exceed 40 mg qd

Pediatric

Not established

Interactions

NSAIDs may reduce hypotensive effects; may increase digoxin, lithium, and allopurinol levels; rifampin decreases levels; probenecid may increase levels; hypotensive effects may be enhanced when administered concurrently with diuretics

Contraindications

Documented hypersensitivity; hyperkalemia; AV block; hypotension; sick sinus syndrome

Precautions

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Caution in renal impairment, valvular stenosis, or severe congestive heart failure; causes increase in serum potassium levels, which require careful monitoring

Diuretics

Treat edema and hypertension. Increase urine excretion by inhibiting sodium and chloride transporters.

Furosemide (Lasix)

DOC as a diuretic. Increases excretion of water by interfering with chloride-binding cotransport system, which, in turn, inhibits sodium and chloride reabsorption in ascending loop of Henle and distal renal tubule.

Dosing

Adult

1-2 mg/kg PO/IV qd/bid; not to exceed 600 mg/d
0.1-0.4 mg/kg/h continuous IV infusion

Pediatric

1-2 mg/kg PO/IV qd/bid; not to exceed 6 mg/kg/dose

Interactions

Metformin decreases concentrations; interferes with hypoglycemic effect of antidiabetic agents and antagonizes muscle-relaxing effect of tubocurarine; auditory toxicity appears to be increased with coadministration with aminoglycosides; hearing loss of varying degrees may occur; anticoagulant activity of warfarin may be enhanced when taken concurrently; increased plasma lithium levels and toxicity are possible when taken concurrently

Contraindications

Documented hypersensitivity; hepatic coma, anuria, and state of severe electrolyte depletion

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Perform frequent serum electrolyte, carbon dioxide, glucose, creatinine, uric acid, calcium, and BUN determinations during first few months of therapy and periodically thereafter

Metolazone (Mykrox, Zaroxolyn)

Treats edema in congestive heart failure. Increases excretion of sodium, water, potassium, and hydrogen ions by inhibiting reabsorption of sodium in distal tubules. May be more effective in impaired renal function.

Dosing

Adult

5-20 mg PO qd

Pediatric

Not established

Interactions

Thiazides may decrease effect of anticoagulants, sulfonylureas, and gout treatments; anticholinergics and amphotericin B may increase toxicity of thiazides; effects of thiazides may decrease when used concurrently with bile acid sequestrants, NSAIDs, or methenamine; when administered concurrently, thiazides increase toxicity of anesthetics, diazoxide, digitoxin, lithium, loop diuretics, antineoplastics, allopurinol, calcium salts, vitamin D, and nondepolarizing muscle relaxants

Contraindications

Documented hypersensitivity; hepatic coma or anuria

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Caution in hepatic or renal disease, diabetes mellitus, gout, or lupus erythematosus

Calcium channel blockers

Treat hypertension, angina, and atrial fibrillation.⁵

Amlodipine (Norvasc)

Blocks slow calcium channels, causing relaxation of vascular smooth muscles.

Dosing

Adult

2.5-10 mg PO qd

Pediatric

Not established

Interactions

May increase effects of benazepril, beta-blockers, and cyclosporine

Contraindications

Documented hypersensitivity; hypotension

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

May cause hypotension, severe left ventricular dysfunction, or sick sinus syndrome; caution in hepatic and renal dysfunction

Nifedipine (Procardia)

Relaxes coronary smooth muscle and produces coronary vasodilation, which, in turn, improves myocardial oxygen delivery. SL administration generally safe, despite theoretical concerns.

Dosing

Adult

Short-acting: 10 mg PO tid
Long-acting: 30 mg PO qd; not to exceed 120-180 mg qd

Pediatric

Not established

Interactions

Caution with coadministration of any agent that can lower blood pressure, including beta-blockers and opioids; H2 blockers (cimetidine) may increase toxicity

Contraindications

Documented hypersensitivity; hypotension; sick sinus syndrome; AV blocks; aortic stenosis; acute MI; cardiogenic shock

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Short-acting forms not recommended for hypertensive emergencies because sudden fall in blood pressure may cause cerebral and cardiac ischemia; may cause lower extremity edema; allergic hepatitis is rare

Beta-adrenergic blockers

Compete with beta-adrenergic agonists for available beta-receptor sites. Propranolol, nadolol, timolol, penbutolol, carteolol, sotalol, and pindolol inhibit both beta-1 receptors (located mainly in cardiac muscle) and beta-2 receptors (located mainly in bronchial and vascular musculature), thus inhibiting chronotropic, inotropic, and vasodilatory responses to beta-adrenergic stimulation.

Metoprolol (Lopressor)

Selective beta1-adrenergic receptor blocker that decreases automaticity of contractions. During IV administration, carefully monitor blood pressure, heart rate, and ECG.

Dosing

Adult

50 mg PO bid, qwk to desired effect; not to exceed 450 mg/d

Pediatric

Not established

Interactions

Aluminum salts, barbiturates, NSAIDs, penicillins, calcium salts, cholestyramine, and rifampin may decrease bioavailability and plasma levels, possibly resulting in decreased pharmacologic effects; toxicity may increase with coadministration of sparfloxacin, phenothiazines, astemizole, calcium channel blockers, quinidine, flecainide, and contraceptives; may increase toxicity of digoxin, flecainide, clonidine, epinephrine, nifedipine, prazosin, verapamil, and lidocaine

Contraindications

Documented hypersensitivity; uncompensated congestive heart failure; bradycardia; asthma; cardiogenic shock; AV conduction abnormalities

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Pregnancy category D in second and third trimesters, beta-adrenergic blockade may reduce signs and symptoms of acute hypoglycemia and may decrease clinical signs of hyperthyroidism; abrupt withdrawal may exacerbate symptoms of hyperthyroidism, including thyroid storm; monitor patient closely and withdraw drug slowly; during IV administration, carefully monitor blood pressure, heart rate, and ECG

Alpha-adrenergic agonists

Used in combination with other agents for management of hypertension.

Clonidine (Catapres)

Stimulates presynaptic (central) alpha-2 agonist, thereby reducing norepinephrine release and peripheral vasoconstriction.

Dosing

Adult

0.1-0.2 mg PO bid/tid; not to exceed 2.4 mg qd

Pediatric

Not established

Interactions

TCAs inhibit hypotensive effects; coadministration with beta-blockers may potentiate bradycardia; TCAs may enhance hypertensive response associated with abrupt clonidine withdrawal; hypotensive effects are enhanced by narcotic analgesics

Contraindications

Documented hypersensitivity; breastfeeding; abrupt discontinuation

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in cerebrovascular disease, coronary insufficiency, sinus node dysfunction, and renal impairment

Follow-up

Further Inpatient Care

Patients with CKD admitted to the hospital should have careful monitoring of weight, intake, output, and renal function so that acute renal failure, if it occurs, can be diagnosed and treated early. All potentially nephrotoxic agents must be adjusted for the degree of CKD. Furthermore, agents, such as nonsteroidal anti-inflammatory drugs (NSAIDs), aminoglycosides, and intravenous contrast, must be avoided, unless the benefits clearly outweigh the risks, because these agents are highly associated with acute renal failure.

Further Outpatient Care

Patients with any evidence of kidney disease should be referred to a kidney specialist (nephrologist). Data suggest that early referral to a nephrologist improves the overall outcome. The nephrologist will usually determine the frequency of visits based on the degree of CKD.

Complications

• The presence of the following complications generally indicates a need for urgent dialysis:
  • Metabolic acidosis
  • Pulmonary edema
  • Pericarditis
  • Uremic encephalopathy
  • Uremic gastrointestinal bleeding
  • Uremic neuropathy
  • Severe anemia and hypocalcemia
  • Hyperkalemia

Prognosis

The prognosis depends on the type of chronic glomerulonephritis (see Causes).

Patient Education

• For further information, see Mayo Clinic - Kidney Transplant Information.
• Dietary education is paramount in managing patients with CKD. The typical dietary restriction is 2 g of sodium, 2 g of potassium, and 40-60 g of protein a day. Additional restrictions may apply for diabetes, hyperlipidemia, and fluid overload.
• Patients should be educated regarding the types of ESRD therapy. The specific choices of ESRD therapy include hemodialysis, peritoneal dialysis, and renal transplantation.
  
  
  • Patients opting for hemodialysis should be educated on home hemodialysis (ie, patients are trained to do their dialysis at home) and center hemodialysis (ie, patients must come to a center 3 times a week for 3.5- to 4-hour dialysis sessions). They should also be educated on the types of vascular access. Arteriovenous fistulae should be created when the GFR falls below 25 mL/min or the serum creatinine level is greater than 4 mg/dL to allow for maturation of the access prior to the initiation of dialysis.
  • Peritoneal dialysis catheters can be placed if dialysis is anticipated within 2-3 weeks.
  • Preemptive transplantation before the initiation of dialysis improves survival as compared with transplantation after the initiation of dialysis; therefore, preemptive transplantation should be explored from live donors. In patients without live donors, they can be placed on the deceased donor wait list when the GFR falls below 20 mL/min to accrue time. Patients who opt for no treatment when it is indicated should be informed of imminent renal failure in a shorter time.
• In the United States and most developed countries, patients on dialysis can travel. In fact, there are even dialysis cruises. However, patients should inform their social workers to make the necessary arrangements prior to any travel to ensure that the destination has the right resources to continue dialysis.
• Sexual dysfunction and loss of libido is common in patients with kidney disease, especially in men. Patients should be told to seek medical therapy if they experience these symptoms.

Miscellaneous

Medicolegal Pitfalls

• Nephrotic (urinary protein excretion, >3.5 g/d) patients may have hyperlipidemia. As a part of cardiovascular health care, lipid profile should be checked and lipid-lowering therapy started for patients with hyperlipidemia.
• Steroid therapy may induce or exacerbate diabetes, hypertension, weight gain, fat redistribution in the trunk (buffalo hump) and face (moon facies), cosmetic problems (eg, hirsutism, acne), and osteoporosis.
  
  
  • Monitor fasting blood glucose levels and blood pressure. Obtain baseline bone densitometry values. Repeat bone densitometry for bone pain.
  • Oral calcium supplements (1 g/d) and vitamin D (400-800 IU/d) are recommended for prophylaxis against osteoporosis.

Special Concerns

• Renal failure and hypertension worsen during pregnancy in patients with CKD, particularly when the serum creatinine level exceeds 2 mg/dL. The result is decreased fetal viability and increased maternal morbidity in pregnant women with CKD. Therefore, women with CKD should consult their doctors prior to pregnancy.

References

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2. Hayakawa K, Ohashi H, Yokoyama H, et al. Adiponectin is increased and correlated with the degree of proteinuria, but plasma leptin is not changed in patients with chronic glomerulonephritis. Nephrology (Carlton). Apr 2009;14(3):327-31. [Medline].

3. Wolf G. Antiproteinuric response to dual blockade of the renin-angiotensin system in primary glomerulonephritis. Nat Clin Pract Nephrol. Sep 2008;4(9):474-5. [Medline].

4. Cho ME, Smith DC, Branton MH, et al. Pirfenidone slows renal function decline in patients with focal segmental glomerulosclerosis. Clin J Am Soc Nephrol. Sep 2007;2(5):906-13. [Medline].

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8. Cameron JS. The Long-Term Outcome of Glomerular Diseases. In: Schrier RW, Gottschalk CW, ed. Diseases of the Kidney. 6^th ed. Little, Brown & Company: Boston, Mass; 1997:1919.

9. Campbell NR, Burgess E, Choi BC, Taylor G, Wilson E, Cléroux J, et al. Lifestyle modifications to prevent and control hypertension. 1. Methods and an overview of the Canadian recommendations. Canadian Hypertension Society, Canadian Coalition for High Blood Pressure Prevention and Control, Lab Centre for Disease Control. CMAJ. May 4 1999;160(9 Suppl):S1-6. [Medline].

10. Contreras G, Pardo V, Leclercq B, Lenz O, Tozman E, O'Nan P, et al. Sequential therapies for proliferative lupus nephritis. N Engl J Med. Mar 4 2004;350(10):971-80. [Medline].

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Keywords

glomerulonephritis, chronic glomerulonephritis, IgA nephropathy, membranous nephropathy, membranoproliferative glomerulonephritis, poststreptococcal glomerulonephritis, glomerulonephritis treatment, crescentic glomerulonephritis, glomerulosclerosis, rapidly progressive glomerulonephritis, RPGN, focal segmental glomerulosclerosis, FSGS, glomerular fibrosis, tubulointerstitial fibrosis, lupus nephritis, azotemia, uremia

Contributor Information and Disclosures

Author

Moro O Salifu, MD, MPH, FACP, Associate Professor, Department of Internal Medicine, Chief, Division of Nephrology, Director of Nephrology Fellowship Program and Transplant Nephrology, State University of New York Downstate Medical Center
Moro O Salifu, MD, MPH, FACP is a member of the following medical societies: American College of Physicians-American Society of Internal Medicine, American Medical Association, American Society for Artificial Internal Organs, American Society of Diagnostic and Interventional Nephrology, American Society of Nephrology, American Society of Transplantation, and National Kidney Foundation
Disclosure: Nothing to disclose.

Coauthor(s)

Barbara G Delano, MD, MPH, Director of Home Hemodialysis and Peritoneal Dialysis, Professor, Department of Internal Medicine, Division of Nephrology, State University of New York at Brooklyn
Barbara G Delano, MD, MPH is a member of the following medical societies: American Society of Nephrology, International Society of Nephrology, National Kidney Foundation, and Sigma Xi
Disclosure: Nothing to disclose.

Medical Editor

Frank C Brosius III, MD, Nephrology Program Director, Professor of Internal Medicine and Physiology, Department of Internal Medicine, Division of Nephrology, University of Michigan School of Medicine
Frank C Brosius III, MD is a member of the following medical societies: Alpha Omega Alpha, American Diabetes Association, American Society of Nephrology, and Phi Beta Kappa
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

George R Aronoff, MD, Director, Professor, Departments of Internal Medicine and Pharmacology, Section of Nephrology, Kidney Disease Program, University of Louisville School of Medicine
George R Aronoff, MD is a member of the following medical societies: American Federation for Medical Research, American Society of Nephrology, Kentucky Medical Association, and National Kidney Foundation
Disclosure: Nothing to disclose.

CME Editor

Rebecca J Schmidt, DO, FACP, FASN, Professor of Medicine, Section Chief, Department of Medicine, Section of Nephrology, West Virginia University School of Medicine
Rebecca J Schmidt, DO, FACP, FASN is a member of the following medical societies: American College of Osteopathic Internists, American College of Physicians, American Medical Association, American Society of Nephrology, International Society of Nephrology, National Kidney Foundation, Renal Physicians Association, and West Virginia State Medical Association
Disclosure: Abbott Grant/research funds Speaking and teaching; Genzyme Honoraria Consulting; Amgen Honoraria Speaking and teaching; Ortho Biotech Honoraria Speaking and teaching

Chief Editor

Vecihi Batuman, MD, FACP, FASN, Professor of Medicine, Section of Nephrology-Hypertension, Tulane University School of Medicine; Chief, Medicine Service, Southeast Louisiana Veterans Health Care System
Vecihi Batuman, MD, FACP, FASN is a member of the following medical societies: American College of Physicians, American Society of Hypertension, American Society of Nephrology, and International Society of Nephrology
Disclosure: Nothing to disclose.

Clinical guidelines:
ACR Appropriateness Criteria® renal failure. American College of Radiology - Medical Specialty Society. 1995 (revised 2008). 10 pages. NGC:007019

Clinical trials:
Efficacy and Safety Study of Abatacept to Treat Lupus Nephritis

Etanercept for the Treatment of Lupus Nephritis

Retinoids for Minimal Change Disease and Focal Segmental Glomerulosclerosis

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