Chronic Glomerulonephritis Treatment & Management

  • Author: Moro O Salifu, MD, MPH, FACP; Chief Editor: Vecihi Batuman, MD, FACP, FASN   more...
 
Updated: Jan 12, 2012
 

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.[6]
    • 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.[7] 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.
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Surgical Care

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

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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.
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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.
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Activity

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

Specialty Editor Board

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.

Francisco Talavera, PharmD, PhD  Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

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.

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 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: Renal Ventures Ownership interest Other

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.

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