Factors that can speed up the decline and cause CKD include: Diabetes, Hypertension, Medications (e.g., NSAIDs or lithium), Glomerulonephritis, Polycystic kidney disease.
Signs and symptoms as the renal function worsens may be non-specific: Fatigue, Pallor (due to anaemia), Foamy urine (proteinuria), Nausea, Loss of appetite, Pruritus (itching), Oedema.
Treating the underlying cause involves optimising diabetic control, optimising hypertension control, reducing or avoiding nephrotoxic drugs (where appropriate), and treating glomerulonephritis (where this is the cause).
A diagnosis can be made when there are consistent results over three months of either: Estimated glomerular filtration rate (eGFR) sustained below 60 mL/min/1.73 m2 or Urine albumin:creatinine ratio (ACR) sustained above 3 mg/mmol.
NICE clinical knowledge summaries (May 2023) suggest referral to a renal specialist when: eGFR less than 30 mL/min/1.73 m2, Urine ACR more than 70 mg/mmol, or 5-year risk of requiring dialysis over 5%.
Dapagliflozin is the SGLT-2 inhibitor licensed for CKD and is offered to patients with diabetes plus a urine ACR above 30 mg/mmol, considered for patients with diabetes plus a urine ACR or 3-30 mg/mmol, and non-diabetics with an ACR of 22.6 mg/mmol or above.
Anaemia in Chronic Kidney Disease is treated with erythropoiesis-stimulating agents, such as recombinant human erythropoietin, and blood transfusions can sensitise the immune system, increasing the risk of future transplant rejection.
Renal bone disease, also known as chronic kidney disease-mineral and bone disorder (CKD-MBD), involves high serum phosphate, low vitamin D activity, low serum calcium, and reduced phosphate excretion.
Management of complications in CKD involves oral sodium bicarbonate to treat metabolic acidosis, iron and erythropoietin to treat anaemia, vitamin D, low phosphate diet and phosphate binders to treat renal bone disease, and dialysis or renal transplant for end-stage renal disease.
ACE inhibitors are offered to all patients with diabetes plus a urine ACR above 3 mg/mmol, hypertension plus a urine ACR above 30 mg/mmol, and all patients with a urine ACR above 70 mg/mmol.
The parathyroid glands react to the low serum calcium and high serum phosphate by excreting more parathyroid hormone, causing secondary hyperparathyroidism.