The Kidney Disease Outcomes Quality Initiative (K/DOQI) of the National Kidney Foundation (NKF) defines Chronic Kidney Disease (CKD) as either kidney damage or a decreased kidney glomerular filtration rate (GFR) of <60>m2, for 3 or more months.
K/DOQI (February 2002) published a classification of the stages of CKD, as follows:
- Stage 1: Kidney damage with normal or increased GFR (>90 mL/min/1.73 m2)
- Stage 2: Mild reduction in GFR (60-89 mL/min/1.73 m2)
- Stage 3: Moderate reduction in GFR (30-59 mL/min/1.73 m2)
- Stage 4: Severe reduction in GFR (15-29 mL/min/1.73 m2)
- Stage 5: Kidney failure (<15>/min/1.73 m2 or dialysis)
Whatever the underlying etiology, the destruction of renal mass with irreversible sclerosis and loss of nephrons leads to a progressive decline in GFR.
- Approximately 1 million nephrons / kidney, each contributing to the total GFR.
- The kidney has an innate ability to maintain GFR by hyperfiltration and compensatory hypertrophy of the remaining healthy nephrons.
- Progressive destruction of nephrons start to show significant increases in urea and creatinine plasma levels only after total GFR has decreased to 50%,
- The plasma creatinine value will double with a 50% reduction in GFR.
- The residual nephron hyperfiltration and hypertrophy has been hypothesized to represent a major cause of progressive renal dysfunction.
- This is believed to occur because of increased glomerular capillary pressure, which damages the capillaries and leads initially to focal and segmental glomerulosclerosis and eventually to global glomerulosclerosis.
- Factors other than the underlying disease process and glomerular hypertension that may cause progressive renal injury include the following :
- US: The US Renal Data System (USRDS) has shown a dramatic increase in patients with CKD who require chronic dialysis or transplantation.
- Internationally: The incidence rates of end-stage renal disease (ESRD) have increased steadily internationally since 1989. The United States has the highest incident rate of ESRD, followed by Japan. Japan has the highest prevalence per million population, with the United States taking second place.
- CKD is a major cause of morbidity and mortality, particularly at the later stages.
- The 5-year survival rate for a patient undergoing chronic dialysis in the United States is approximately 35%. This is approximately 25% in patients with diabetes.
- Although the diabetic population is at highest risk, in the United States, the most common cause of death in the dialysis population is Cardiovascular Disease.
- CKD affects all races, but, in the United States, a significantly higher incidence of ESRD exists in blacks as compared to whites; the incident rate for blacks is nearly 4 times that for whites.
- In NHANES III : The distribution of estimated GFRs for the CKD stages was similar in both sexes.
- Nonetheless, the USRDS 2004 Annual Data Report reveals that the incident rate of ESRD cases is higher for males with 409 per million population in 2002 compared to 276 for females.
- CKD is found in all ages. Especially in geriatric patient with DM or hypertension.
- In the United States, the highest incidence rate of ESRD occurs in patients > 65 years (The Geriatric Population).
- 11% had CKD stage 3 or worse according to the NHANES III was found on US population older than 65 years without diabetes mellitus or hypertension.
- After age 30 years progressive physiological glomerulosclerosis occurs
- GFR (and creatinine clearance [CrCl) falling linearly at a rate of approximately 8 cc/min/1.73 m2/y from a maximal GFR of 140 cc/min/1.73 m2.
- Aging also results in concomitant progressive physiological decrease in muscle mass such that daily urinary creatinine excretion
- This combination of factors results in constant serum creatinine values over time in a given individual, despite a decrease in CrCl (and GFR).
CrCl must be calculated simply by using the Cockcroft-Gault formula in elderly people so that appropriate drug dosing adjustments can be made and nephrotoxins can be avoided in patients who have more extensive CKD than would be suggested by the serum creatinine alone.
- Simptomatic in patient with stage 4 and 5 CKD (GFR <30
- Hyperkalemia (in patient with GFR <20-25>
- Metabolic Acidosis (non–anion gap and anion gap)
- In CKD the kidneys are unable to produce enough ammonia in the proximal tubules to excrete the endogenous acid into the urine in the form of ammonium.
- In CKD stage 5, accumulation of phosphates, sulphates, and other organic anions are the cause of the small anion gap.
- Extracellular volume expansion and total-body volume overload
- Results from failure of sodium and free water excretion.
- Failed compensatory mechanisms present patient with peripheral and, not uncommonly, pulmonary edema and hypertension.
- Normochromic normocytic anemia
- Develops from Decreased Synthesis of Erythropoietin, the hormone responsible for bone marrow stimulation for red blood cell (RBC) production.
- It becomes more severe as GFR progressively decreases with the availability of less viable renal mass. No reticulocyte response occurs. RBC survival is decreased, and tendency of bleeding is increased from the uremia-induced platelet dysfunction.
- Secondary Hyperparathyroidism
- Hypocalcemia develops primarily from decreased intestinal calcium absorption because of low plasma calcitriol levels and possibly from calcium binding to elevated serum levels of phosphate.
- If serum levels of PTH remain elevated, a high–bone turnover lesion, known as osteitis fibrosa, develops. This is one of several bone lesions, which as a group are commonly known as renal osteodystrophy.
- Other Manifestations (More likely in patients who are inadequately dialyzed) :
- Encephalopathy - Can progress to coma and death
- Peripheral neuropathy, Restless leg syndrome
- GI symptoms - Anorexia, nausea, vomiting, diarrhea
- Skin manifestations - Dry skin, pruritus, ecchymosis
- Fatigue, increased somnolence, failure to thrive, Malnutrition
- Erectile dysfunction, decreased libido, amenorrhea
- Platelet dysfunction with tendency to bleeding
- Lab Studies:
- Elevated serum urea and creatinine
- Hyperkalemia, low serum bicarbonate, hypocalcemia, hyperphosphatemia, hyponatremia (in ESRD with free-water excess)
- Hypoalbuminemia in patients who are nephrotic and/or malnourished
- Normochromic normocytic anemia - Rule out other underlying causes of anemia.
- Urinalysis
- Twenty-four–hour urine collection for total protein and CrCl
- Serum and urine protein electrophoresis to screen for multiple myeloma (a monoclonal protein)
- Antinuclear antibodies (ANA), to screen for systemic lupus erythematosus. Serum complement levels - May be depressed with some glomerulonephritides
- C-ANCA and P-ANCA levels - Helpful if positive in diagnosis of Wegener granulomatosis and polyarteritis nodosa or microscopic polyangiitis, respectively
- Anti–glomerular basement membrane (anti-GBM) antibodies - Highly suggestive of underlying Goodpasture syndrome
- Hepatitis B and C, HIV, Venereal Disease Research Laboratory (VDRL) serology - Conditions associated with some glomerulonephritides
- Imaging Studies:
- Intravenous Pyelogram - Not commonly (potential renal toxicity)
- Retrograde pyelogram may be indicated if a high index of clinical suspicion for obstruction exists despite a negative study finding.
- Renal Radionuclide Scan - To screen for renal artery stenosis when performed with captopril administration
- CT scan - To better define renal masses and cysts usually noted on ultrasound.
- It is the most sensitive test for identifying renal stones.
- IV contrast-enhanced CT scans should be avoided in patients with renal impairment and dehydration to avoid acute renal failure.
- MRI - Useful in patients who require a CT scan but who cannot receive IV contrast.
- It is reliable in the diagnosis of renal vein thrombosis,
- Alternatively, the Modification of Diet in Renal Disease (MDRD) Study equation could be used to calculate GFR. This equation does not require a patient's weight (Levey, 1999).
- Vascular disease - Renal artery stenosis, cytoplasmic pattern antineutrophil cytoplasmic antibody (C-ANCA)–positive and perinuclear pattern antineutrophil cytoplasmic antibody (P-ANCA)–positive vasculitides, antineutrophil cytoplasmic antibody (ANCA)–negative vasculitides, atheroemboli, hypertensive nephrosclerosis, renal vein thrombosis
- Primary glomerular disease - Membranous nephropathy, immunoglobulin A (IgA) nephropathy, focal and segmental glomerulosclerosis (FSGS), minimal change disease, membranoproliferative glomerulonephritis, rapidly progressive (crescentic) glomerulonephritis
- Secondary glomerular disease - Diabetes mellitus, systemic lupus erythematosus, rheumatoid arthritis, mixed connective tissue disease, scleroderma, Goodpasture syndrome, Wegener granulomatosis, mixed cryoglobulinemia, postinfectious glomerulonephritis, endocarditis, hepatitis B and C, syphilis, human immunodeficiency virus (HIV), parasitic infection, heroin use, gold, penicillamine, amyloidosis, light chain deposition disease, neoplasia, thrombotic thrombocytopenic purpura (TTP), hemolytic-uremic syndrome (HUS), Henoch-Schönlein purpura, Alport syndrome, reflux nephropathy
- Tubulointerstitial disease - Drugs (eg, sulfa, allopurinol), infection (viral, bacterial, parasitic), Sjögren syndrome, chronic hypokalemia, chronic hypercalcemia, sarcoidosis, multiple myeloma cast nephropathy, heavy metals, radiation nephritis, polycystic kidneys, cystinosis
- Urinary tract obstruction - Urolithiasis, benign prostatic hypertrophy, tumors, retroperitoneal fibrosis, urethral stricture, neurogenic bladder
Diferential Diagnosis
- Treatment of the underlying condition if possible
- Aggressive blood pressure control to target values per current guidelines
- Use of ACE inhibitors as tolerated, with close monitoring for renal deterioration and for hyperkalemia (avoid in advanced renal failure, bilateral renal artery stenosis [RAS], RAS in a solitary kidney)
- Aggressive glycemic control per the American Diabetes Association (ADA) recommendations; target HbA1C <7.0%>
- Protein restriction - Controversial
- Treatment of hyperlipidemia to target levels per current guidelines
- Avoidance of nephrotoxins - IV radiocontrast, nonsteroidal anti-inflammatory agents, aminoglycosides
- Anemia with erythropoietin
- Hyperphosphatemia with dietary phosphate binders and restriction
- Hypocalcemia with calcium supplements +/- calcitriol
- Hyperparathyroidism with calcitriol or vitamin D analogs
- Volume overload with loop diuretics or ultrafiltration
- Metabolic acidosis with oral alkali supplementation
- Uremic manifestations with chronic renal replacement therapy (hemodialysis, peritoneal dialysis, or renal transplantation):
- Indications include severe metabolic acidosis, hyperkalemia, pericarditis, encephalopathy, intractable volume overload, failure to thrive and malnutrition, peripheral neuropathy, intractable gastrointestinal symptoms, and GFR less than 10 mL/min.
- Cardiovascular complications
- Early education
- About disease progression, different dialytic modalities, renal transplantation, patient option to refuse or discontinue chronic dialysis
- Timely placement of permanent vascular access
- Arrange for surgical creation of primary arteriovenous fistula, if possible, and preferably at least 6 months in advance of anticipated date of dialysis)
- Timely elective peritoneal dialysis catheter insertion
- Timely referral for renal transplantation
- Protein restriction early in CKD to delay a decline in GFR (Controversial)
- Phosphate restriction starting early in CKD
- Potassium restriction
Medication
- Phosphate-lowering agent
- Hyperphosphatemia - Dietary phosphate binders and dietary phosphate restriction.
- Hypocalcemia - Calcium supplements and possibly calcitriol.
- Hyperparathyroidism - calcitriol or vitamin D analogs.
- Ca Supplement (Calcium acetate, Calcium carbonate), Vit D (Calcitriol), Doxercalciferol (Vit D Analog), Lanthanum carbonate (Inhibiting Phosphorus Absorption). Sevelamer (Renagel) (Inhibiting Phosphorus Absorption)
- Iron salts -- Nutritionally essential inorganic substances used to treat anemia.
- Ferrous sulfate (Feosol, Feratab, Slow FE)
- Iron dextran (DexFerrum, InFed) -- Used to treat microcytic, hypochromic anemia resulting from iron deficiency when oral administration is unfeasible or ineffective.
- Ferric gluconate (Ferrlecit) -- Replaces iron found in hemoglobin, myoglobin, and specific enzyme systems. Allows transportation of oxygen via hemoglobin.
Source
Edited By C14
No comments:
Post a Comment