Chronic Kidney Disease (CKD) Overview

• Chronic kidney disease (CKD) is the progressive loss of renal function and the destruction of nephrons in both kidneys.
• Systemic diseases like diabetes mellitus, hypertension, or lupus erythematosus are risk factors of CKD.
• Intrinsic kidney diseases, such as AKI, chronic glomerulonephritis, chronic pyelonephritis, obstructive uropathies, and vascular disorders are also risk factors of CKD.
• Diabetes (38%) and renal vascular disease (15%) are known leading causes of CKD.
• Acute kidney injury (AKI) can progress to CKD.
• Kidney damage: GFR less than 60 mL/min for 3 months or more, irrespective of cause based on the Canadian Medical Association and the US National Kidney Foundation.
• Chronic kidney disease is the preferred terminology to describe a gradual loss of kidney function and declining GFR.
• GFR >90 mL/min is considered normal kidney function.
• GFR 60 to 89 mL/min is considered mild kidney damage.
• GFR 30 to 59 mL/min is considered moderate kidney damage.
• GFR 15 to 29 mL/min is considered severe kidney damage.
• GFR <15 is considered end-stage kidney disease.

Progression of Chronic Kidney Disease

• Glomerular hyperfiltration of protein contributes to tubular interstitial injury and progressive fibrosis.
• In CKD, GFR falls and plasma creatinine concentration increases.
• Plasma creatinine levels continue to rise and serve as an index of changing glomerular function, because there is no regulatory adjustment for creatinine.
• Urea clearance increases as GFR declines.
• In CKD, sodium load to nephrons exceeds normal, so excretion must increase.
• Obligatory loss leads to sodium deficits and volume depletion.
• Ability to concentrate and dilute urine diminishes as GFR is reduced.
• Major disorders associated with CKD are reduced renal phosphate excretion, decreased renal synthesis of 1,25-dihydroxy-vitamin D3, and hypocalcemia.
• Hypocalcemia leads to secondary hyperparathyroidism, GFR falls, and progressive hyperphosphatemia, hypocalcemia, and dissolution of bone result.
• With accompanying anemia, lethargy, dizziness, and low hematocrit are common.
• Tubular secretion of potassium increases until oliguria develops.
• Use of potassium-sparing diuretics may precipitate elevated serum potassium levels.
• Total body potassium levels can rise to life-threatening levels and dialysis is required as disease progresses.
• Metabolic acidosis begins when GFR reaches 30-40%.
• Metabolic acidosis and hyperkalemia may be severe enough to require dialysis when end-stage kidney disease develops.
• Chronic dyslipidemia may induce glomerular and tubulointerstitial injury, contributing to progression of CKD.

Clinical Manifestations

• Skeletal system effects lead to spontaneous fractures, bone pain, and deformities of long bones.
• Osteitis fibrosa: bone inflammation with fibrous degeneration related to hyperparathyroidism.
• Osteomalacia: bone resorption associated with vitamin D and calcium deficiency
• Cardiopulmonary effects include pulmonary edema and Kussmaul respirations.
• Fluid overload is associated with pulmonary edema and metabolic acidosis, leading to Kussmaul respirations.
• Cardiovascular effects include left ventricular hypertrophy, cardiomyopathy, and ischemic heart disease, hypertension, dysrhythmias, accelerated atherosclerosis; pericarditis with fever, chest pain, and pericardial friction rub
• Extracellular volume expansion and hypersecretion of renin associated with hypertension; anemia increases cardiac workload; dyslipidemia promotes atherosclerosis; toxins precipitate into pericardium.
• Neurological effects include encephalopathy (fatigue, reduced attention span, difficulty with problem solving); peripheral neuropathy (pain and burning in legs and feet, loss of vibration sense and deep tendon reflexes); loss of motor coordination, twitching, fasciculations, stupor, and coma with advanced uremia.
• Progressive accumulation of uremic toxins associated with end-stage kidney disease (ESKD).
• Stroke or intracerebral hemorrhage is associated with chronic dialysis
• Hematological effects include anemia (usually normochromic-normocytic) and platelet disorders with prolonged bleeding times.
• Reduced erythropoietin secretion and reduced red cell production; uremic toxins shorten red blood cell survival and alter platelet function.
• Gastro-intestinal effects include anorexia, nausea, vomiting; mouth ulcers, stomatitis, urine odour of breath (uremic fetor), hiccups, peptic ulcers, gastro-intestinal bleeding, and pancreatitis associated with ESKD.
• Retention of metabolic acids and other metabolic waste products.
• Integumentary effects include abnormal pigmentation and pruritus.
• Retention of urochromes contributes to a sallow yellow colour; high plasma calcium levels and neuropathy associated with pruritus.
• Immunological effects include an increased risk for infection that can cause death and an increased risk for carcinoma.
• Suppression of cell-mediated immunity; reduction in the number and function of lymphocytes, diminished phagocytosis
• Reproductive effects include sexual dysfunction: menorrhagia, amenorrhea, infertility, and decreased libido in women; decreased testosterone levels, infertility, and decreased libido in men.
• Dysfunction of ovaries and testes; presence of neuropathies.

Nursing Assessment

• PMH: history of any existing renal disease or family history of renal disease, hypertension, diabetes, recurrent urinary tract infections, and systemic lupus erythematosus
• Medications: (kidneys play a large role in the absorption, distribution, metabolism, and elimination of drugs and because many drugs are potentially nephrotoxic)
• Dietary habits and discuss any problems.
• Height and weight should be measured, and any recent weight changes must be evaluated.
• Clinical manifestations of CKD are apparent in multiple body systems: Fatigue, lethargy, and pruritus, hypertension, urine changes are often the early symptoms of CKD.
• Support systems should be assessed. CKD affects family relationships, social and work activities, and self-image and emotional state.
• GFR: glomerular filtration or the number of ml of filtrate made by the kidney per minute
• BUN (elevated with kidney dx or dehydration from lack of blood flow to kidneys (Prerenal))
• Serum creatinine is also elevated.
• eGFR (low filtration rate from kidney damage, injury) Does not provide a useful estimate of filtration in a setting of rapidly changing kidney function, such as in acute kidney failure.
• Serum calcium is low in CKD.
• Phosphorus is increased in CKD.
• Serum electrolytes, hyperkalemia (>6.5mEq/L) and hyponatremia (<125mEq/L).
• Decreased Bicarb: metabolic acidosis
• Serum hemoglobin level and iron indices.
• Urinalysis: proteinuria, microalbuminuria is one of the most important risk factors for the progression of CKD (earliest maker for kidney damage)
• Preferred method to screen for proteinuria is the measurement of the protein-to-creatinine ratio in first, morning-voided specimen.
• Diagnostics: dx polycystic kidney disease, renal artery stenosis, and hydronephrosis
• Renal ultrasound, CT scan, Renal biopsy show causes of CKD.

Additional Notes on Hormones and Renal Issues

• ADH increases water permeability and reabsorption in the last segment of the distal tubule and along the entire length of the collecting ducts.
• ANP inhibits secretion of renin, inhibits angiotensin-induced secretion of aldosterone, relaxes vascular smooth muscle, and inhibits sodium and water absorption by kidney tubules.
• Renin is secreted to raise blood pressure.
• Aldosterone regulates water and sodium balance.
• Obstruction can occur anywhere in the urinary tract, and it may be anatomical or functional, including renal stones, an enlarged prostate gland, urethral strictures, or neurogenic bladder.
• The most serious complications are hydronephrosis, hydroureter, ureterohydronephrosis, and infection caused by the accumulation of urine behind the obstruction.

Obstructive Uropathy

• Urinary tract obstruction is an interference with the flow of urine at any site along the urinary tract
• Obstruction of the upper urinary tract causes dilation of the ureter, renal pelvis, calyces, and renal parenchyma proximal to the site of urinary blockage resulting from a “backing up” of urine.
• The increased pressure is transmitted to the glomerulus, which decreases filtration.
• Partial obstruction of the bladder can result in overactive bladder (OAB) contractions with urgency.
• Deposition of collagen in the bladder wall can occur over time, resulting in decreased bladder wall compliance and ineffective detrusor muscle contraction.
• Obstructive disorders of the lower urinary tract are primarily related to storage of urine in the bladder or emptying of urine through the bladder outlet.
• Lower urinary tract obstruction: urethral stricture, prostate enlargement, and pelvic organ prolapse in women.
• Incontinence is a common symptom for lower urinary tract disorders

Types of Incontinence

• Urge incontinence (most common in older adults) - Involuntary loss of urine associated with abrupt and strong desire to void (urgency); often associated with involuntary contractions of the detrusor
• Stress incontinence (most common in women <60 years and men who have had prostate surgery) - Involuntary loss of urine during coughing, sneezing, laughing, or other physical activity associated with increased abdominal pressure
• Overflow incontinence - Involuntary loss of urine with overdistension of bladder; associated with neurological lesions below S1, polyneuropathies, and urethral obstruction (e.g., enlarged prostate)
• Mixed incontinence (most common in older women) - Combination of both stress and urge incontinence
• Functional incontinence - Involuntary loss of urine attributable to dementia or immobility

Other Renal Issues

• Neurogenic Bladder: Bladder dysfunction caused by neurological damage.
• Pyelonephritis: An infection of one or both upper urinary tracts (ureter, renal pelvis, and interstitium often related to obstructive uropathies and may cause abscess formation and scarring with an alteration in renal function.
• Acute pyelonephritis: Acute infection of the ureter, renal pelvis, interstitium
• Causes: Vesicoureteral reflux, E. coli, Proteus, Pseudomonas
• Chronic pyelonephritis: Episodes of acute pyelonephritis that lead to scarring
• Increased risk of chronic pyelonephritis in individuals with renal infections and some type of obstructive pathological condition
• Glomerulonephritis: Glomerular disorders that can be caused by immune responses, toxins or medications, vascular disorders, and other systemic diseases.
• Inflammation of the glomerulus from immunological abnormalities
• Acute glomerulonephritis results from inflammatory damage to the glomerular filtration membrane as a consequence of immune reactions (e.g., after a streptococcal infection).
• Diabetic nephropathy is the most common cause of glomerular injury progressing to chronic kidney disease (CKD).
• Chronic glomerulonephritis is related to a variety of diseases that cause deterioration of the glomerulus and a progressive loss of renal function.
• Hypercholesterolemia and proteinuria are associated with progressive glomerular and tubular injury.
• Diabetes mellitus and lupus erythematosus are examples of secondary causes of chronic glomerular injury
• Renal insufficiency usually begins to develop after 10 to 20 years, followed by nephrotic syndrome and an accelerated progression to ESKD.

Chronic Kidney Disease

• CKD is the progressive loss of renal function.
• Plasma creatinine levels gradually become elevated as GFR declines;
• Sodium is lost in the urine;
• Potassium is retained;
• Acidosis develops;
• Calcium and phosphate metabolism are altered; and
• Erythropoietin production is diminished.
• All organ systems are affected by CKD.