Chronic renal failure overview

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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] Kosar Doraghi, M.D. [3]

Overview

Chronic renal failure (CRF), also known as chronic kidney failure (CKF) or chronic kidney disease (CKD), or chronic renal insufficiency (CRI) is a slowly progressive loss of renal function over a period of months or years defined as an abnormally low glomerular filtration rate. The glomerular filtration rate is usually determined indirectly by the creatinine level in blood serum.

CRF that leads to severe illness and requires some form of renal replacement therapy (such as dialysis) is called end-stage renal disease (ESRD).

Definition

• CKD is defined as:
  • Presence of markers of kidney damage for > 3 months, and may include abnormalities in markers in blood or urine, and imaging tests.
  • GFR < 60 mL/min/1.73 m2 for > 3 months with or without other signs of kidney damage.

Pathophysiology

CRF begins with damage to the nephrons, the filtering units of the kidneys, due to diseases such as diabetes, hypertension, immune complex deposition, toxin exposure, and inflammation. To compensate for the decreased glomerular filtration rate by the damaged nephrons, healthy nephrons hypertrophy and start hyperfiltrating due to signals from the body. As the disease process progresses, this adaptive response becomes maladaptive, and the increased filtration pressure in the healthy nephrons leads to the distortion of its structural architecture, causing sclerosis and eventual dropout of these nephrons.

Epidemiology and Demographics

The incidence and prevalence of chronic renal failure varies enormously depending on the level of affluence of the country. Developed countries have higher incident rates of treated end-stage renal failure, whereas emerging countries have very low incident rates. People with disorders that have adverse effects on the kidneys such as diabetes, and hypertension have increased chances of developing CRF.

Risk Factors

Disorders or habits that damage small blood vessels or the nephrons are risk factors for developing chronic renal failure. Some of the factors associated with CRF include diabetes, hypertension, autoimmune diseases, obesity, smoking, high cholesterol, heart disease, and racial background.

Causes

CRF is associated with diseases such as diabetic nephropathy, hypertension, glomerulonephritis, ischemic nephropathy, vasculitis, Hemolytic-uremic syndrome, IgA nephropathy, and polycystic kidney disease to name a few. Diseases of the blood vessels or diseases that damage the nephrons are usually linked to the development of CRF.

Differentiating Chronic renal failure from other Conditions

CRF can be discerned from acute renal failure by looking at the timeline of the rise of serum creatinine levels. Acute renal failure is identified by sharp rises in the levels of creatinine, while CRF is identified by a slow and gradual increase in serum creatinine.

Natural History, Complications and Prognosis

Repeated episodes of acute renal injury from infections, drugs, toxins and immunological damage may accelerate the progression to chronic renal failure, especially in the elderly. Once CRF is developed, the condition can cause systemic problems such as infertility, myopathy, sleep disorders, pruritis, congestive heart failure, and pulmonary edema amongst other problems. The prognosis and quality of life for a patient with CRF is poor. Data indicates that the overall death rate increases as kidney function decreases.

Diagnosis

Symptoms

Some symptoms of CRF include: malaise, pruritus, headaches, drowsiness, numbness of the hands and feet, vomiting, bone pain, abnormally dark or light skin, and sleep disorders to name a few.

Physical Examination

Chronic renal failure causes disturbances not only in the filtration function of the kidney, but also in the normal functioning of virtually every organ in the body. Symptoms and overt signs of kidney disease are often subtle or are absent until renal failure ensues. Thus, the diagnosis of chronic renal failure often takes the patient by surprise and may cause denial.

Laboratory Studies

The kidneys play an important role in the regulation of serum concentration of sodium, potassium, calcium, phosphate, bicarbonate and chloride as well as levels of hemoglobin, hematocrit, blood pressure and extracellular volume. Hence, chronic injury to the kidneys can lead to abnormalities in the stable values of the above mentioned parameters.

Treatment

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.

Recommendations of the KDIGO 2024 Clinical Practice Guideline for Evaluation and Management of CKD(DO NOT EDIT)

Detection and evaluation of CKD (DO NOT EDIT)

Class I

"1. (In adults at risk for CKD, we recommend using creatinine-based estimated glomerular filtration rate (eGFRcr). If cystatin C is available, the GFR category should be estimated from the combination of creatinine and cystatin C (creatinine and cystatin C– based estimated glomerular filtration rate eGFRcr-cys) (Level of Evidence: B)"

Evaluation of chronicity and cause (DO NOT EDIT)

Class II

"1. (We suggest performing a kidney biopsy as an acceptable, safe, diagnostic test to evaluate cause and guide treatment decisions when clinically appropriate) (Level of Evidence: D)"

Evaluation of GFR(DO NOT EDIT)

Class I

"1. (We recommend using eGFRcr-cys in clinical situations when eGFRcr is less accurate and GFR affects clinical decision-making class) (Level of Evidence: C)"

Point-of-care testing (DO NOT EDIT)

Class II

"1. (We suggest that point-of-care testing (POCT) may be used for creatinine and urine albumin measurement where access to a laboratory is limited or providing a test at the point-of-care facilitates the clinical pathway) (Level of Evidence: C)"

Risk prediction in people with CKD (DO NOT EDIT)

Class I

"1. (In people with CKD G3–G5, we recommend using an externally validated risk equation to estimate the absolute risk of kidney failure) (Level of Evidence: A)" A 5-year kidney failure risk of 3%–5% can be used to determine need for nephrology referral in addition to criteria based on eGFR or urine ACR, and other clinical considerations. A 2-year kidney failure risk of >10% can be used to determine the timing of multidisciplinary care in addition to eGFR-based criteria and other clinical considerations. A 2-year kidney failure risk threshold of >40% can be used to determine the modality education, timing of preparation for kidney replacement therapy (KRT) including vascular access planning or referral for transplantation, in addition to eGFR-based criteria and other clinical considerations. Note that risk prediction equations developed for use in people with CKD G3–G5, may not be valid for use in those with CKD G1–G2.

Physical activity and optimum weight (DO NOT EDIT)

Class I

"1. (We recommend that people with CKD be advised to undertake moderate-intensity physical activity for a cumulative duration of at least 150 minutes per week, or to a level compatible with their cardiovascular and physical tolerance) (Level of Evidence: D)"

Sodium intake (DO NOT EDIT)

Class II

"1. (We suggest that sodium intake be <2 g of sodium per day (or <90 mmol of sodium per day, or <5 g of sodium chloride per day) in people with CKD) (Level of Evidence: C)"

Blood pressure control (DO NOT EDIT)

Class II

"1. (We suggest that adults with high BP and CKD be treated with a target systolic blood pressure (SBP) of <120 mm Hg, when tolerated, using standardized office BP measurement) (Level of Evidence: B)"

Pediatric considerations (DO NOT EDIT)

Class II

"1. (We suggest that in children with CKD, 24-hour mean arterial pressure (MAP) by ambulatory blood pressure monitoring (ABPM) should be lowered to <50th percentile for age, sex, and height) (Level of Evidence: C)"

Delaying CKD progression and managing its complications (DO NOT EDIT)

Renin-angiotensin system inhibitors (DO NOT EDIT)

Class I

"1. (We recommend starting renin-angiotensin-system inhibitors (RASi) (angiotensin-converting enzyme inhibitor or angiotensin II receptor blocker) for people with CKD and severely increased albuminuria (G1–G4, A3) without diabetes) (Level of Evidence: B)"

Class II

"1. (We suggest starting RASi (ACEi or ARB) for people with CKD and moderately increased albuminuria (G1–G4, A2) without diabetes) (Level of Evidence: C)"

Class I

"1. (We recommend starting RASi (ACEi or ARB) for people with CKD and moderately-to-severely increased albuminuria (G1–G4, A2 and A3) with diabetes) (Level of Evidence: B)"

”2. (We recommend avoiding any combination of ACEi, ARB, and direct renin inhibitor (DRI) therapy in people with CKD, with or without diabetes) (Level of Evidence: B)"

Sodium-glucose cotransporter-2 inhibitors (DO NOT EDIT)

Class I

"1. (We recommend treating patients with type 2 diabetes, CKD, and an eGFR >20 ml/min per 1.73 m2 with an SGLT2i ) (Level of Evidence: A)"

Mineralocorticoid receptor antagonists (MRA) (DO NOT EDIT)

Class I

"1. (We suggest a nonsteroidal mineralocorticoid receptor antagonist with proven kidney or cardiovascular benefit for adults with T2D, an eGFR >25 ml/min per 1.73 m2, normal serum potassium concentration, and albuminuria (>30 mg/g >3 mg/mmol) despite maximum tolerated dose of RAS inhibitor) (Level of Evidence: A)"

Glucagon-like peptide-1 receptor agonists (GLP-1 RA) (DO NOT EDIT)

Class I

"1. (In adults with T2D and CKD who have not achieved individualized glycemic targets despite use of metformin and SGLT2 inhibitor treatment, or who are unable to use those medications, we recommend a long-acting GLP-1 RA) (Level of Evidence: B)"

Hyperuricemia (DO NOT EDIT)

Class I

"1. (We recommend people with CKD and symptomatic hyperuricemia should be offered uric acid–lowering intervention) (Level of Evidence: C)"

Class II

"1. (We suggest not using agents to lower serum uric acid in people with CKD and asymptomatic hyperuricemia to delay CKD progression) (Level of Evidence: D)"

Cardiovascular disease (CVD) and additional specific interventions to modify risk (DO NOT EDIT)

Class I

"1. (In adults aged ≥50 years with eGFR <60 ml/min per 1.73 m2 but not treated with chronic dialysis or kidney transplantation (GFR categories G3a–G5), we recommend treatment with a statin or statin/ezetimibe combination) (Level of Evidence: A)"

”2. (In adults aged ≥50 years with CKD and eGFR ‡60 ml/min per 1.73 m2 (GFR categories G1–G2), we recommend treatment with a statin ) (Level of Evidence: B)"

Class II

"1. (In adults aged 18–49 years with CKD but not treated with chronic dialysis or kidney transplantation, we suggest statin treatment in people with one or more of the following : known coronary disease (myocardial infarction or coronary revascularization), diabetes mellitus, prior ischemic stroke, or estimated 10-year incidence of coronary death or nonfatal myocardial infarction >10%) (Level of Evidence: A)"

Recommendations of the KDIGO 2024 Clinical Practice Guideline for Evaluation and Management of CKD(DO NOT EDIT)

Use of antiplatelet therapy(DO NOT EDIT)

Class I

"1. (We recommend oral low-dose aspirin for prevention of recurrent ischemic cardiovascular disease events (i.e., secondary prevention) in people with CKD and established ischemic cardiovascular disease ) (Level of Evidence: C)"

Invasive versus intensive medical therapy for coronary artery disease(DO NOT EDIT)

Class II

"1. (We suggest that in stable stress-test confirmed ischemic heart disease, an initial conservative approach using intensive medical therapy is an appropriate alternative to an initial invasive strategy ) (Level of Evidence: D)"

CKD and atrial fibrillation(DO NOT EDIT)

Class I

"1. (We recommend use of non–vitamin K antagonist oral anticoagulants (NOACs) in preference to vitamin K antagonists (e.g., warfarin) for thromboprophylaxis in atrial fibrillation in people with CKD G1–G4) (Level of Evidence: C)"

Sources

• 2024 the KDIGO 2024 Clinical Practice Guideline for the Evaluation and Management of Chronic Kidney Disease.

References

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