Chronic renal failure medical therapy: Difference between revisions
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*Generally, [[angiotensin converting enzyme inhibitor]]s ([[ACEI]]s) or [[angiotensin II receptor blockers]] (ARBs) are used, as they have been found to slow the progression of [[CRF]] by reducing intra-glomerular pressure.<ref>Ruggenenti P, Perna A, Gherardi G, Gaspari F, Benini R, Remuzzi G. Renal function and requirement for dialysis in chronic nephropathy patients on long-term ramipril: REIN follow-up trial. Gruppo Italiano di Studi Epidemiologici in Nefrologia (GISEN). Ramipril Efficacy in Nephropathy. Lancet. 1998 Oct 17;352(9136):1252-6. PMID 9788454.</ref><ref>Ruggenenti P, Perna A, Gherardi G, Garini G, Zoccali C, Salvadori M, Scolari F, Schena FP, Remuzzi G. Renoprotective properties of ACE-inhibition in non-diabetic nephropathies with non-nephrotic proteinuria. Lancet. 1999 Jul 31;354(9176):359-64. PMID 10437863.</ref> Thus, the more effective a drug is in reducing protein filtration into renal tubules, the greater is the impact on improving [[GFR]]. | *Generally, [[angiotensin converting enzyme inhibitor]]s ([[ACEI]]s) or [[angiotensin II receptor blockers]] (ARBs) are used, as they have been found to slow the progression of [[CRF]] by reducing intra-glomerular pressure.<ref>Ruggenenti P, Perna A, Gherardi G, Gaspari F, Benini R, Remuzzi G. Renal function and requirement for dialysis in chronic nephropathy patients on long-term ramipril: REIN follow-up trial. Gruppo Italiano di Studi Epidemiologici in Nefrologia (GISEN). Ramipril Efficacy in Nephropathy. Lancet. 1998 Oct 17;352(9136):1252-6. PMID 9788454.</ref><ref>Ruggenenti P, Perna A, Gherardi G, Garini G, Zoccali C, Salvadori M, Scolari F, Schena FP, Remuzzi G. Renoprotective properties of ACE-inhibition in non-diabetic nephropathies with non-nephrotic proteinuria. Lancet. 1999 Jul 31;354(9176):359-64. PMID 10437863.</ref> Thus, the more effective a drug is in reducing protein filtration into renal tubules, the greater is the impact on improving [[GFR]]. | ||
*[[Angiotensin converting enzyme inhibitors]] act by inhibiting [[angiotensin]] mediated vasoconstriction of efferent arterioles, thereby reducing filtration pressures and [[proteinuria]]. | *[[Angiotensin converting enzyme inhibitors]] act by inhibiting [[angiotensin]] mediated vasoconstriction of efferent arterioles, thereby reducing filtration pressures and [[proteinuria]]. | ||
*Combination of [[ACE inhibitor]]s and [[ARB]]'s is associated with greater reduction in [[proteinuria]] than either drug used alone. | *Combination of [[ACE inhibitor]]s and [[ARB]]'s is associated with greater reduction in [[proteinuria]] than either drug used alone. | ||
*Side effects include [[cough]] and [[angioedema]] with [[ACE inhibitor]]s, whereas [[anaphylaxis]] and [[hyperkalemia]] is common to use of both [[ACE inhibitors]] and [[ARB]]'s. Progressive increase in [[serum creatinine]] levels suggests concomitant [[renovascular disorder]]s. | |||
*Development of the above mentioned side effects may warrant use of other [[antihypertensive]] agents like calcium channel blockers like [[diltiazem]] and [[verapamil]]. | |||
*If [[proteinuria]] is strongly associated with the disease progression, like in [[diabetic nephropathy]] or glomerular disease, [[ACE inhibitor]]s should be the first line drugs, whereas in diseases like [[polycystic kiney disease]] and [[tubulointerstitial diseases]] in which there is minimal or absent [[proteinuria]], other [[antihypertensive]] agents may be used. | |||
* | ==Control of blood glucose== | ||
*Tight glycemic control reduces the risk of progression of [[diabetic nephropathy]]. Ideally, the blood glucose levels should be between 90-130 mg/dL(5.0-7.2 mmol/L) and [[hemoglobin A1c]] below 7%. | |||
* | *If the [[GFR]] progressively decreases inspite of tight glycemic control, the use and dose of [[oral hypoglycemics]] have to be reevaluated. | ||
* | *In presence of renal compromise, [[chlorpropamide]] has an exaggerated hypoglycemic effect, [[metfromin]] can cause [[lactic acidosis]] and [[thiazolidinediones]] may aggravate volume overload states. | ||
*Renal degradation of administered [[insulin]] decreases with reduction in [[GFR]] and hence the need to reduce the dose for appropriate glucose control. | |||
==References== | ==References== | ||
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Aarti Narayan, M.B.B.S [2]
Overview
Treatment is aimed at specific causes of chronic renal failure. It includes optimized glucose levels in patients with diabetes, management of blood pressure, immunomodulators for glomerulonephritis, emerging specific therapies to retard cytogenesis in polycystic kidney disease and replacement of critical hormones and chemicals produced and utilized by normally healthy kidneys. Any acceleration in the disease process should prompt a search for superimposed acute or subacute disease process that is potentially reversible. These include extravascular fluid volume depletion, urinary tract infection, obstructive uropathy, exposure to nephrotoxic agents such as NSAIDs or radiocontrasts, re-activation and flare of the primary disease like SLE or vasculitis.
Blood pressure management
- The goal of therapy is to slow down or halt the otherwise relentless progression of CRF.
- In addition to reducing the cardiovascular disease risk, use of antihypertensive therapy in patients with CRF also aims at slowing the progression of nephron injury by reducing intra-glomerular hypertension.
- Elevated blood pressure increases albuminuria by increasing its flux through the renal capillaries.
- Generally, angiotensin converting enzyme inhibitors (ACEIs) or angiotensin II receptor blockers (ARBs) are used, as they have been found to slow the progression of CRF by reducing intra-glomerular pressure.[1][2] Thus, the more effective a drug is in reducing protein filtration into renal tubules, the greater is the impact on improving GFR.
- Angiotensin converting enzyme inhibitors act by inhibiting angiotensin mediated vasoconstriction of efferent arterioles, thereby reducing filtration pressures and proteinuria.
- Combination of ACE inhibitors and ARB's is associated with greater reduction in proteinuria than either drug used alone.
- Side effects include cough and angioedema with ACE inhibitors, whereas anaphylaxis and hyperkalemia is common to use of both ACE inhibitors and ARB's. Progressive increase in serum creatinine levels suggests concomitant renovascular disorders.
- Development of the above mentioned side effects may warrant use of other antihypertensive agents like calcium channel blockers like diltiazem and verapamil.
- If proteinuria is strongly associated with the disease progression, like in diabetic nephropathy or glomerular disease, ACE inhibitors should be the first line drugs, whereas in diseases like polycystic kiney disease and tubulointerstitial diseases in which there is minimal or absent proteinuria, other antihypertensive agents may be used.
Control of blood glucose
- Tight glycemic control reduces the risk of progression of diabetic nephropathy. Ideally, the blood glucose levels should be between 90-130 mg/dL(5.0-7.2 mmol/L) and hemoglobin A1c below 7%.
- If the GFR progressively decreases inspite of tight glycemic control, the use and dose of oral hypoglycemics have to be reevaluated.
- In presence of renal compromise, chlorpropamide has an exaggerated hypoglycemic effect, metfromin can cause lactic acidosis and thiazolidinediones may aggravate volume overload states.
- Renal degradation of administered insulin decreases with reduction in GFR and hence the need to reduce the dose for appropriate glucose control.
References
- ↑ Ruggenenti P, Perna A, Gherardi G, Gaspari F, Benini R, Remuzzi G. Renal function and requirement for dialysis in chronic nephropathy patients on long-term ramipril: REIN follow-up trial. Gruppo Italiano di Studi Epidemiologici in Nefrologia (GISEN). Ramipril Efficacy in Nephropathy. Lancet. 1998 Oct 17;352(9136):1252-6. PMID 9788454.
- ↑ Ruggenenti P, Perna A, Gherardi G, Garini G, Zoccali C, Salvadori M, Scolari F, Schena FP, Remuzzi G. Renoprotective properties of ACE-inhibition in non-diabetic nephropathies with non-nephrotic proteinuria. Lancet. 1999 Jul 31;354(9176):359-64. PMID 10437863.