Early intervention can improve outcomes in acute kidney injury.

The incidence of acute kidney injury (AKI) is rising reflecting an increasingly elderly at-risk population, with multiple comorbidities, coupled with improved detection of AKI following introduction of clinical chemistry laboratory algorithms. AKI is potentially reversible so improvements in its recognition and early interventions could have a major impact on patient outcomes. AKI occurs when there is a rapid decrease in GFR within hours to days. The loss of kidney function results in the retention of urea and creatinine and subsequent dysregulation of electrolytes and fluid balance. Individuals in the community with pre-existing CKD and/or patients treated with an ACE inhibitor or angiotensin receptor blocker are at increased risk of AKI if they develop an illness associated with hypovolaemia or hypotension. Potential clues in the history for AKI include reduced fluid intake and/or increased fluid losses, urinary tract symptoms and recent drug ingestion. Postural changes in pulse and BP are more sensitive indicators of hypovolaemia than supine observations. Once an unexplained raised serum creatinine is identified this should trigger a careful review of the patient's history including the common AKI risk factors, medication record, baseline renal function and clinical examination. The severity of the AKI should be considered by evaluating the extent of rise of serum creatinine from baseline. Reagent strip urinalysis should be performed, if possible, on any patient with suspected AKI. Positive protein and blood indicators of 2+ to 4+ on urinalysis suggest intrinsic glomerular disease and should trigger more urgent referral to hospital. The focus of AKI management is correcting the conditions causing or contributing to it.

Improving early detection of chronic kidney disease.

Chronic kidney disease (CKD) is defined as either a reduction in measured kidney function (eGFR) or urinary abnormalities (haematuria/proteinuria) or a combination of both, present for more than 3 months. In the most recent NICE guidelines the various CKD stages 1-5 are now represented by G (for GFR) categories (G1-5) which have the same eGFR thresholds as previous CKD guidelines. The urinary albumin:creatinine ratio (ACR) category is denoted as A (for albuminuria) with three categories: A1, A2 or A3. The ACR category has been introduced to emphasise that patients with higher levels of albuminuria have an increased risk of progression to end-stage renal disease. Individuals with newly identified reduced eGFR should have acute kidney injury excluded. All newly identified CKD patients should have blood pressure, dipstick urinalysis, random urine ACR or urine protein:creatinine ratio (PCR), glucose, cholesterol and full blood count checked at the earliest opportunity. An ultrasound scan should be offered to patients at increased risk. Cardiovascular events and progression of CKD are more common if albuminuria or proteinuria is present. Urine ACR has a greater sensitivity for low levels of proteinuria in comparison with PCR. Referral for patients with CKD should be based on assessment of kidney function (eGFR), the severity of proteinuria (urine ACR), concerns about poorly controlled BP, or suspected inherited renal disease. Most cases of CKD in the elderly are caused by the cumulative effect of other disease states, especially hypertension and atherosclerosis. The CKD classification system will identify many elderly patients with a low eGFR but without progressive kidney failure.

The challenges of antiphospholipid syndrome: experience from diagnosis to self-care.

A young woman presented to our unit with pancreatitis and acute kidney injury (AKI) 4 weeks after initiation of an oral contraceptive. She subsequently developed seizures due to posterior reversible encephalopathy syndrome and required ongoing haemodialysis for oliguric AKI. Routine antiphospholipid antibody screen was normal, but arterial and venous thromboses were identified on renal biopsy. Further coagulation studies identified an antiphospholipid-dependent inhibitor confirming the suspected diagnosis of antiphospholipid syndrome. She remained seizure free with control of hypertension and was established on anticoagulation. She remained haemodialysis dependent performing this independently at a new self-care unit. She provides us with valuable insights into her experience encouraging us to reconsider our current methods of education and communication in our younger population of patients living with chronic disease.