Causes span chronic infections (glomerulonephritis, pyelonephritis), vascular disease (hypertension, nephrosclerosis), obstruction (renal calculi), collagen disease (systemic lupus), nephrotoxic agents (drugs such as aminoglycosides), and endocrine disease (diabetes, hyperparathyroidism). CRF is the final common pathway of many kidney and urinary tract diseases.
CKD is common and often silent. It affects about 1 in 7 US adults, roughly 35.5 million people, and most of them do not know they have it because symptoms rarely show up until the later stages. Diabetes is the leading cause, accounting for about 45% of new cases of kidney failure, followed by high blood pressure (CDC).
Pathophysiology
Each underlying disease has its own mechanism, but progression follows common paths. Pathology includes fibrosis, loss of renal cells, and infiltration of renal tissue by monocytes and macrophages. Proteinuria, hypoxia, and heavy angiotensin II production all drive injury. Trying to maintain GFR, the glomerulus hyperfilters, which injures the endothelium. Proteinuria results from increased glomerular permeability and capillary pressure. Hypoxia adds to the damage, and angiotensin II raises glomerular hypertension, which damages the kidney further.
Predisposing factors: diabetes (the most common risk factor for chronic kidney failure in the United States), age 60 or older, congenital kidney disease, family history of kidney disease, autoimmune disorder (lupus erythematosus), bladder outlet obstruction (BPH, prostatitis), and race (sickle cell disease). Precipitating factors: occupational toxin or medication overexposure, sedentary lifestyle (hypertension, atherosclerosis), and a high-residue diet.
Clinical Manifestations
Nearly every system is affected in ESRD. Peripheral neuropathy shows up in some patients with severe pain and discomfort. Restless leg syndrome and burning feet can appear in the early stage of uremic peripheral neuropathy.
Complications
Watch for and manage these collaboratively. Hyperkalemia from decreased excretion, metabolic acidosis, catabolism, and excessive intake (diet, medications, fluids). Pericarditis from retained uremic waste and inadequate dialysis. Hypertension from sodium and water retention and a malfunctioning renin-angiotensin-aldosterone system. Anemia from decreased erythropoietin production, shortened RBC lifespan, GI bleeding from irritating toxins and ulcers, and blood loss during hemodialysis. Bone disease with metastatic and vascular calcifications from phosphorus retention, low serum calcium, abnormal vitamin D metabolism, and elevated aluminum levels.
Assessment and Diagnostic Findings
GFR and creatinine clearance fall while serum creatinine (the more sensitive indicator of renal function) and BUN rise. Some patients retain sodium and water, raising the risk of edema, heart failure, and hypertension. Metabolic acidosis develops because the kidneys cannot excrete the acid load. Erythropoietin production drops and profound anemia follows, bringing fatigue, angina, and shortness of breath.
Urine: volume usually less than 400 mL/24 hr (oliguria) or absent (anuria). Color may be cloudy from pus, bacteria, fat, colloidal particles, phosphates, or urates; dirty brown sediment points to RBCs, hemoglobin, myoglobin, or porphyrins. Specific gravity less than 1.015, fixed at 1.010 with severe renal damage. Osmolality less than 350 mOsm/kg signals tubular damage, with a urine/serum ratio often 1:1. Creatinine clearance may drop sharply (less than 80 mL/min in early failure, less than 10 mL/min in ESRD). Sodium more than 40 mEq/L because the kidney cannot reabsorb it. High-grade proteinuria (3 to 4+) strongly suggests glomerular damage when RBCs and casts are also present.
Blood: BUN and creatinine are elevated in proportion; creatinine of 12 mg/dL suggests ESRD and BUN over 25 mg/dL indicates renal damage. Hgb is decreased from anemia, usually less than 7 to 8 g/dL, with shortened RBC lifespan from erythropoietin deficiency and azotemia. ABGs show decreased pH; metabolic acidosis (less than 7.2) occurs as the kidney loses the ability to excrete hydrogen, ammonia, and protein-catabolism end products, with decreased bicarbonate and PCO2. Serum sodium may be low (if the kidney wastes sodium) or normal (reflecting the dilutional state). Potassium is elevated from retention and cellular shifts (acidosis) or tissue release (RBC hemolysis); in ESRD, ECG changes may not appear until potassium reaches 6.5 mEq or higher, and potassium may instead be low on potassium-wasting diuretics or with dialysis. Magnesium and phosphorus are elevated; calcium and phosphorus may be decreased. Albumin and other proteins fall from urinary loss, fluid shifts, low intake, or decreased synthesis from a lack of essential amino acids. Serum osmolality is higher than 285 mOsm/kg, often equal to urine.
Imaging and procedures: KUB x-ray shows kidney, ureter, and bladder size and obstruction (stones). Retrograde pyelogram outlines renal pelvis and ureter abnormalities. Renal arteriogram assesses circulation and identifies extravascularities and masses. Voiding cystourethrogram shows bladder size, reflux into ureters, and retention. Renal ultrasound determines kidney size and detects masses, cysts, and upper-tract obstruction. Renal biopsy may be done endoscopically for histologic diagnosis. Renal endoscopy or nephroscopy examines the renal pelvis, flushes out calculi, clears hematuria, and removes selected tumors. ECG may be abnormal, reflecting electrolyte and acid-base imbalances. X-rays of feet, skull, spinal column, and hands may show demineralization or calcifications from the electrolyte shifts of CRF.
Medical Management
Preserve kidney function and homeostasis as long as possible. Pharmacologic therapy: calcium and phosphorus binders treat hyperphosphatemia and hypocalcemia; antihypertensive and cardiovascular agents (digoxin and dobutamine) manage hypertension; anti-seizure agents (IV diazepam or phenytoin) treat seizures; and erythropoietin (Epogen) treats the anemia of ESRD. Nutritional therapy carefully regulates protein, matches fluid intake to losses, matches sodium to losses, and restricts potassium. Dialysis starts when conservative treatment can no longer support a reasonable lifestyle.
Nursing Management
ESRD demands sharp nursing care to head off the complications of failing renal function and the stress of a life-threatening illness.
Assessment. Check fluid status (daily weight, intake and output, skin turgor, neck vein distention, vital signs, respiratory effort), dietary patterns (diet history, food preference, calorie counts), nutritional status (weight changes, labs), the patient's understanding of the cause, consequences, and treatment of renal failure, the patient's and family's responses to illness and treatment, and for signs of hyperkalemia.
Diagnosis. Common nursing diagnoses: excess fluid volume related to decreased urine output, dietary excess, and sodium and water retention; imbalanced nutrition less than body requirements related to anorexia, nausea, vomiting, dietary restriction, and altered oral mucous membranes; activity intolerance related to fatigue, anemia, retained waste, and dialysis; and risk for situational low self-esteem related to dependency, role changes, body image, and sexual function.
Planning and goals: maintain ideal body weight without excess fluid, maintain adequate nutrition, participate in activity within tolerance, and improve self-esteem.
Nursing priorities: maintain homeostasis, prevent complications, teach the disease process and treatment needs, and support adjustment to lifestyle changes.
Interventions. Assess fluid status and find sources of imbalance. Run a dietary program that meets nutrition within the regimen's limits. Promote self-care and independence. Push high-biologic-value protein (eggs, dairy, meats). Schedule medications so they do not land immediately before meals. Alternate activity with rest.
Evaluation. The plan succeeds when the patient maintains ideal body weight without excess fluid, maintains adequate nutrition, participates in activity within tolerance, and improves self-esteem.
Discharge and Home Care Guidelines
Teach vascular access care: check the access device for patency and avoid venipuncture and blood pressure measurements on the access arm. Tell the patient and family which problems to report: nausea, vomiting, change in usual urine output, ammonia odor on the breath, muscle weakness, diarrhea, abdominal cramps, a clotted fistula or graft, and signs of infection. Stress followup exams and treatment because physical status, renal function, and dialysis requirements keep changing. A home care referral lets the nurse assess the patient's environment, emotional status, and family coping.
Documentation Guidelines
Document existing conditions and the degree of fluid retention, intake and output and fluid balance, lab results, caloric intake, cultural or religious restrictions and personal preferences, level of activity, the plan of care, the teaching plan, responses to interventions and teaching, progress toward outcomes, modifications to the plan, and long-term needs.
Frequently Asked Questions
What is chronic renal failure? It is the gradual, progressive, and irreversible loss of kidney function over months to years. When the kidneys can no longer clear metabolic waste or carry out their regulatory work, those substances build up in the blood and cause widespread fluid, electrolyte, acid-base, and hormonal problems. The end point is stage 5 CKD, or kidney failure, which needs dialysis or transplant (National Kidney Foundation).
What is the difference between CRF, CKD, and ESRD? Chronic kidney disease (CKD) is the umbrella term for kidney damage or reduced GFR lasting at least three months. Chronic renal failure refers to the advanced, progressive loss of function within that spectrum. End-stage renal disease (ESRD), or stage 5 CKD, is the final stage where GFR falls below 15 mL/min/1.73 m² and the patient needs renal replacement therapy to stay alive.
What causes chronic kidney disease? Diabetes is the leading cause, responsible for about 45% of new kidney-failure cases, followed by high blood pressure. Other causes include glomerulonephritis, polycystic and other congenital kidney diseases, recurrent obstruction or infection, autoimmune disease such as lupus, and long-term exposure to nephrotoxic drugs (CDC).
How common is chronic kidney disease? It affects about 1 in 7 US adults, an estimated 35.5 million people, and roughly 9 in 10 of them are unaware they have it because early CKD usually has no symptoms (CDC).
What are the major complications nurses watch for? Hyperkalemia, metabolic acidosis, fluid overload and hypertension, anemia from reduced erythropoietin, renal bone disease from disordered calcium and phosphorus, and cardiovascular problems such as pericarditis and heart failure. These are managed collaboratively and monitored closely through labs and daily weights.
Can chronic renal failure be cured? No. The kidney damage is permanent, so the goal is to slow progression, control blood pressure and blood sugar, manage complications, and prepare for dialysis or transplant when function reaches kidney failure. Early detection and tight management of diabetes and hypertension are the most effective ways to protect remaining function.