Complications
Hyperkalemia is common in patients with kidney disease, due to the kidney's inability to excrete potassium from the diet as the estimated glomerular filtration rate declines. Hyporeninaemic hypoaldosteronism due to diabetes may be present and increases the risk of hyperkalaemia. Most patients with hyperkalaemia are asymptomatic, but some may present with muscle weakness.
In advanced chronic kidney disease (CKD), uncontrolled hyperkalaemia indicates need for dialysis.
DKD is complicated by a triad of inflammation, endothelial dysfunction, and oxidative stress and is associated with marked cardiovascular (CV) morbidity and mortality. Raised albuminuria levels are associated with higher risk of incident stroke, myocardial infarction, and all-cause mortality in patients with type 2 diabetes without overt CV disease.[227]
Angina pectoris and CV disease are common in DKD, and are reasons to aggressively treat coronary artery disease with stent/coronary artery bypass graft (CABG) and to intensify treatment of DKD.[228]
American Diabetes Association guidelines recommend considering aspirin for primary prevention of cardiovascular events in men and women aged ≥50 years with diabetes and at least one additional major risk factor, which includes chronic kidney disease (CKD)/albuminuria, who are not at increased risk of bleeding (e.g., older age, anaemia, or renal disease).[1]
Use of a sodium-glucose cotransporter-2 (SGLT2) inhibitor (if estimated glomerular filtration rate [eGFR] is ≥20 mL/minute/1.73 m²), a glucagon-like peptide-1 (GLP-1) receptor agonist, or a non-steroidal mineralocorticoid receptor antagonist (if eGFR is ≥25 mL/minute/1.73 m²) may be considered in those with type 2 diabetes and chronic kidney disease (CKD) to reduce risk of cardiovascular events.[1]
With progressive loss of kidney function, hypertension becomes very difficult to control. Resistant hypertension is defined as blood pressure that remains above target despite the use of three antihypertensive medications of different classes (typically a calcium-channel blocker, an ACE inhibitor, or an angiotensin-II receptor antagonist, and a diuretic) at optimal doses.
Managing recalcitrant hypertension requires expertise; referral to a specialist in hypertension should be considered.
As in all patients with chronic kidney disease (CKD), diabetic patients with CKD often develop secondary hyperparathyroidism due to hyperphosphataemia and vitamin D deficiency.[229] Treatment includes phosphorus (and protein) restriction, phosphate binders (including calcium carbonate, calcium acetate, sevelamer, lanthanum carbonate), and vitamin D replacement, generally with ergocalciferol in early stages of CKD and calcitriol or an active analogue (such as paricalcitol) in later stages.
Compared with people without diabetes, patients with diabetes mellitus are more likely to have adynamic bone disease.[230]
As chronic kidney disease (CKD) progresses, there is a progressive increase in the prevalence and severity of anaemia. Iron indices should be obtained and iron deficiency treated.
Erythropoietic stimulating agents (ESAs) (e.g., epoetin alfa, darbepoetin) are indicated to reduce the need for blood transfusions.
Although there is some variability in results among studies, the CHOIR and CREATE trials indicate better outcomes in patients with CKD who have haemoglobin (Hb) values between 110-120 g/L, or between 11-12 g/dL (i.e., haematocrit between 33% and 36%) compared with values above this range.[231][232] Thus, normalisation of Hb values is not recommended. However, in another study, improvement in quality of life was noted with near-normal Hb in diabetic patients with CKD, so the issue is not completely settled.[233]
Treatment includes iron compounds (ferrous sulfate, iron dextran, ferric gluconate, iron sucrose) and ESAs. ESAs should be avoided in a Hb >130 g/L (13 g/dL) due to increased risk of cardiovascular events.
Intensive treatment of hyperglycaemia may result in hypoglycaemia because of impaired gluconeogenesis and because insulin and other oral hypoglycaemics are poorly cleared by the kidney. One nationwide study, in the US, of patients with diabetes and end-stage kidney disease found that hypoglycaemic crises occurred at a rate of 54 per 1000 person-years.[226] Reduction in antidiabetic treatment is warranted.
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