genitourinary disorders
Chronic Kidney Disease
Treatment of Chronic Kidney Disease
Control of underlying disorders Possible restriction of dietary protein, phosphate, and potassium Vitamin Dsupplements Treatment of anemia Treatment of contributing comorbidities (eg, heart failure, diabetes mellitus, nephrolithiasis, prostatic hypertrophy) Doses of all medications adjusted as needed Maintainingsodium bicarbonatelevel in the normal range (23–29 mmol/L) Dialysis for severely decreased glomerular filtration rate (GFR) if symptoms and signs not adequately managed by medical interventions Underlying disorders and contributory factors must be controlled. In particular, controlling hyperglycemia in patients with diabetic nephropathy and controlling hypertension in all patients substantially slows deterioration of GFR. receptor blockers (ARBs) decrease the rate of decline in GFR in patients with most causes of chronic kidney disease (CKD), particularly those with proteinuria. Increasing evidence suggests that, compared with either medication alone, combined use of ACE inhibitors and ARBs increases incidence of complications and does not slow decline in renal function, even though combined use does reduce Proteinuria more. Sodium-glucose cotransporter-2 (SGLT2) inhibitors delay progression of proteinuric CKD in patients with or without diabetes, although these medications are contraindicated in patients with type 1 diabetes mellitus ( Activityneed not be restricted, although fatigue and lassitude usually limit a patient’s capacity for exercise. Pruritusmay respond to dietary phosphate restriction and phosphate binders if serum phosphate is elevated. without Overview of Nephrotic Syndrome is safe and easy for most patients to tolerate. Some experts recommend 0.6 g/kg/day for patients with diabetes and for patients without diabetes if GFR is Because dietary restrictions may reduce necessary vitamin intake, patients should take a multivitamin containing water-soluble vitamins. Administration of vitamins A and E is unnecessary. Vitamins D2 (ergocalciferol) or D3 (cholecalciferol) are not given routinely but are used based on blood levels ofvitamin D25-OH and PTH. Dyslipidemia should be addressed. Dietary modification may be helpful for hypertriglyceridemia. Statins are effective for hypercholesterolemia. Fibric acid derivatives (clofibrate, Based on updated KDIGO (Kidney Disease Improving Global Outcomes) 2017 clinical practice guidelines ( Treatment references ), it is recommended that serum levels of calcium, phosphate, PTH, Hyperphosphatemia should be treated with Dietary phosphate restriction Phosphate binders . Additional intestinal phosphate binders (calcium-containing or non–calcium-containing) may be necessary for adequate control of hyperphosphatemia, which has been associated with increased cardiovascular risk. Non–calcium-containing binders are preferred in patients with Hypercalcemia , suspected adynamic bone disease, or evidence of vascular calcification on imaging. If calcium-containing binders are prescribed, then the total dietary and medication sources of calcium should not exceed 2000 mg/day in patients with eGFR Vitamin D Deficiency and Dependency should be treated with cholecalciferol (vitamin D3) or ergocalciferol (vitamin D2) to target serum The optimal level of PTH in patients with CKD stages 3a to 5 not on Overview of Renal Replacement Therapy is not known. However, if PTH levels are progressively rising or are markedly elevated (above 9 times the upper limit of normal for the assay), despite treatment of hyperphosphatemia and Restricted water intakeis required only when serum sodium concentration is<135 mmol/L or there is heart failure or severe edema. who have Hypertension , . Treatment of mild to moderate Hyperkalemia (5.1 to 6 mmol/L) entails dietary restriction (including avoiding salt substitutes), correction of metabolic acidosis, and use of potassium-lowering diuretics and gastrointestinal cation exchangers. Metabolic Acidosis None Anemia of Chronic Disease is a common complication of moderate to advanced CKD ( Because of increased iron utilization with stimulated erythropoiesis, iron stores must be replaced, often requiring parenteral iron. Iron concentrations, iron-binding capacity, and ferritin concentrations should be followed closely. Target transferrin saturation (TSAT), calculated by dividing serum iron by total iron binding capacity and multiplying by 100%, should be>20%. Target ferritin in patients not on dialysis is>100 ng/mL. Transfusion should not be done unless anemia is severe (Hb<8 g/dL) or causes symptoms. The bleeding tendency in CKD rarely needs treatment. Cryoprecipitate, red blood cell transfusions,desmopressin0.3 to 0.4 mcg/kg (20 mcg maximum) in 20 mL of isotonic saline IV over 20 to 30 minutes, orconjugated estrogens2.5 to 5 mg orally once a day help when needed. The effects of these treatments last 12 to 48 hours, except forconjugated estrogens, which may last for several days. Symptomatic heart failure is treated with Sodium restriction Diuretics None Sometimes, dialysis usually are effective even when renal function is markedly reduced, although large doses may be needed. If left ventricular function is depressed, Angiotensin-Converting Enzyme (ACE) Inhibitors (or Moderate or severe Hypertension should be treated to avoid its deleterious effects on cardiac and renal function. Patients who do not respond to sodium restriction (1.5 g/day), should receive diuretics. Loop diuretics (eg, Occasionally, dialysis may be required to control heart failure. If reduction of the volume of extracellular fluid does not control blood pressure, conventional antihypertensives are added. Azotemia may increase with such treatment and may be necessary for adequate control of heart failure and/or hypertension. . Hemodialysis reduces the serum concentrations of some medications, which should be supplemented after hemodialysis. It is strongly recommended that physicians consult a reference on drug dosing in renal failure before prescribing medications to these very vulnerable patients ( Most experts recommend avoiding NSAIDs (nonsteroidal anti-inflammatory drugs) in patients with CKD because they may worsen renal function, exacerbate hypertension, and precipitate electrolyte disturbances. . The MRI contrast agent gadolinium has been associated with the development of Disadvantages of MRI in patients with estimated GFR Dialysis is usually initiated at the onset of either of the following: Uremic symptoms (eg, anorexia, nausea, vomiting, weight loss, pericarditis, pleuritis) Difficulty controlling fluid overload, hyperkalemia, or acidosis with medications and lifestyle interventions 15 mL/min in a patient with diabetes; patients whose estimated GFR values are near these values should be closely monitored so that these signs and symptoms are recognized early. Dialysis is best anticipated so that preparations can be made and urgent insertion of a hemodialysis catheter can be avoided. Such preparations usually begin when the patient is in early to mid stage 4 CKD; preparation allows time for patient education, selection of the type of dialysis, and timely creation of an Arteriovenous Fistula or placement of a Begin preparation for dialysis, kidney transplantation, or palliative care during early to mid stage 4 CKD to allow adequate time for patient education and selection of treatment modality, along with any associated preparatory procedures. If a living kidney donor is available, better long-term outcomes occur when a patient receives the transplanted kidney early, even before beginning dialysis. Patients who are transplant candidates but have no living donor should be placed on the waiting list of their regional transplant center early because wait times may exceed several years in many regions of the United States. 1.Perkovic V, Jardine MJ, Neal B, et al:Canagliflozinand renal outcomes in type 2 diabetes and nephropathy.N Engl J Med380(24):2295-2306, 2019. doi: 10.1056/NEJMoa1811744 2.Heerspink HJL, Stefánsson BV, Correa-Rotter R, et al:Dapagliflozinin patients with chronic kidney disease.N Engl J Med383(15):1436-1446, 2020. doi: 10.1056/NEJMoa2024816 3.KDIGO 2017 Clinical Practice Guidelines for the Diagnosis, Evaluation, Prevention, and Treatment of Chronic Kidney Disease–Mineral and Bone Disorder (CKD-MBD)Kidney Int Suppl7(1):1-59, 2017. 4.Determining Drug Dosing in Adults with Chronic Kidney Disease. 5.Munar MY, Singh HD: Drug dosing adjustments in patients with chronic kidney disease.Am Fam Physician75:1487-1496, 2007. 6.Matzke GR, Aronoff GR, Atkinson AJ, et al: Drug dosing consideration in patients with acute and chronic kidney disease—a clinical update from Kidney Disease: Improving Global Outcomes (KDIGO).Kidney Int80:1122–1137, 2011. doi:10.1038/ki.2011.322 7.ACR Committee on Drugs and Contrast Media: ACR Manual on Contrast Media. American College of Radiology. 2021. ISBN: 978-1-55903-012-0 