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CHRONIC KIDNEY DISEASE

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Chronic kidney disease (CKD) is defined as abnormalities in kidney structure or function, present for 3 months or longer, with implications for health. Structural abnormalities include albuminuria of more than 30 mg/day, presence of hematuria or red cell casts in urine sediment, electrolyte and other abnormalities due to tubular disorders, abnormalities detected by histology, structural abnormalities detected by imaging, or history of kidney transplant.

• CKD is classified by cause of kidney disease, glomerular filtration rate (GFR) category, and albuminuria level based on new recommendations from the Kidney Disease: Improving Global Outcomes (KDIGO) guidelines, referred to as CGA staging (cause, GFR, albuminuria)

• CKD stage 5, previously referred to as end-stage renal disease (ESRD), occurs when the GFR falls below 15 mL/min/1.73 m2 (<0.14 mL/s/m2) or in patients receiving renal replacement therapy (RRT). In this chapter, ESRD refers specifically to patients who receive chronic dialysis.


• Prognosis depends on cause of kidney disease, GFR at time of diagnosis, degree of albuminuria, and presence of other comorbid conditions.

PATHOPHYSIOLOGY

Susceptibility factors increase the risk for kidney disease but do not directly cause kidney damage. They include advanced age, reduced kidney mass and low birth weight, racial or ethnic minority, family history, low income or education, systemic inflammation, and dyslipidemia.

Initiation factors directly result in kidney damage and are modifiable by drug therapy. They include diabetesmellitus, hypertension, glomerulonephritis, polycystic kidney disease, Wegener granulomatosis, vascular diseases, and human immunodeficiency virus (HIV) nephropathy.

Progression factors hasten the decline in kidney function after initiation of kidney damage. They include glycemia indiabetics, hypertension, proteinuria, hyperlipidemia, obesity, and smoking.

• Most progressive nephropathies share a final common pathway to irreversible renal parenchymal damage and ESRD. Key pathway elements include loss of nephron mass, glomerular capillary hypertension, and proteinuria.

CLINICAL PRESENTATION




• CKD development and progression are insidious. Patients with stage 1 or 2 CKD usually do not have symptoms or metabolic derangements seen with stages 3 to 5, such as anemia, secondary hyperparathyroidism, cardiovascular disease (CVD), malnutrition, and fluid and electrolyte abnormalities that are more common as kidney function deteriorates.

• Uremic symptoms (fatigue, weakness, shortness of breath, mental confusion, nausea, vomiting, bleeding, and anorexia) are generally absent in stages 1 and 2, minimal during stages 3 and 4, and common in patients with stage 5 CKD who may also experience itching, cold intolerance, weight gain, and peripheral neuropathies.

• Signs and symptoms of uremia are foundational to the decision to implement RRT.

TREATMENT

• Goal of Treatment: The goal is to delay the progression of CKD, minimizing the development or severity of complications.

• Use the most current consensus guidelines and the best clinical practices for management of CKD.

NONPHARMACOLOGIC THERAPY

• Restrict protein to 0.8 g/kg/day if GFR is less than 30 mL/min/1.73 m2.
• Encourage smoking cessation to slow progression of CKD and reduce the risk of CVD.
• Encourage exercise at least 30 minutes five times per week and achievement of a body mass index (BMI) of 20 to 25 kg/m2.

Treatment

• Dietary phosphorus restriction, dialysis, and parathyroidectomy are nonpharmacologic approaches to management of hyperphosphatemia and CKD-MBD.

• The KDOQI guidelines provide desired ranges of calcium, phosphorus, calciumphosphorus product, and intact PTH based on the stage of CKD.

PHOSPHATE-BINDING AGENTS

• Phosphate-binding agents decrease phosphorus absorption from the gut and are first-line agents for controlling both serum phosphorus and calcium concentrations

• KDOQI guidelines recommend that elemental calcium from calcium-containing binders should not exceed 1500 mg/day, and the total daily intake from all sources should not exceed 2000 mg. This may necessitate a combination of calcium- and non–calcium-containing products (eg, sevelamer HCL and lanthanum carbonate).

• Adverse effects of all phosphate binders are generally limited to GI effects, including constipation, diarrhea, nausea, vomiting, and abdominal pain. Risk of hypercalcemia may necessitate restriction of calcium-containing binder use and/or reduction in dietary intake. Aluminum and magnesium binders are not recommended for regular use in CKD because aluminum binders have been associated with CNS toxicity and the worsening of anemia, whereas magnesium binders may lead to hypermagnesemia and hyperkalemia.

VITAMIN D THERAPY

• Reasonable control of calcium and phosphorus must be achieved before initiation and during continued vitamin D therapy.

Calcitriol, 1,25-dihydroxyvitamin D3, directly suppresses PTH synthesis and secretion and upregulates vitamin D receptors. The dose depends on the stage of CKD

• The newer vitamin D analogues paricalcitol and doxercalciferol may be associated with less hypercalcemia and, for paricalcitol, hyperphosphatemia. Vitamin D therapy, regardless of agent, is associated with decreased mortality.

CALCIMIMETICS

Cinacalcet reduces PTH secretion by increasing the sensitivity of the calciumsensing receptor. The most common adverse events include nausea and vomiting.

• The most effective way to use cinacalcet with other therapies has not been decided. The starting dose is 30 mg daily, which can be titrated to the desired PTH and calcium concentrations every 2 to 4 weeks to a maximum of 180 mg daily.

Hyperlipidemia

• The prevalence of hyperlipidemia increases as renal function declines.

• National guidelines differ on how aggressively dyslipidemia should be managed in patients with CKD. KDIGO guidelines recommend treatment with a statin (eg, atorvastatin 20 mg, fluvastatin 80 mg, rosuvastatin 10 mg, simvastatin 20 mg) in adults aged 50 and older with stage 1 to 5 CKD not on dialysis.

• In patients with ESRD, lipid profile should be reassessed at least annually and 2 to 3 months after changing treatment.


CHRONIC KIDNEY DISEASE CHRONIC KIDNEY DISEASE Reviewed by gafacom on April 25, 2019 Rating: 5

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