British Journal of Renal Medicine - 2020

In 1964 Baruch Blumberg recognised that individuals transfused with blood from another individual develop antibodies against the donor’s serum proteins when they differ slightly from their own. These ‘isoprecipitins’ could be identified by their ability to precipitate the protein or antigen. Most of these isoprecipitins reacted with serum lipoproteins, but an isoprecipitin was also identified that reacted with an as yet unidentified protein. This isoprecipitin was found in patients who had received multiple blood transfusions, and was commoner in certain populations including Australian aborigines (Blumberg, 1964).¹

Millions of people worldwide have end-stage kidney disease (ESKD) and need renal replacement therapy (RRT). According to the 21st annual report of the UK renal registry, there were 64,887 adult patients receiving RRT at the end of 2017, among which 39.7% were on hemodialysis (HD).

Having a chronic kidney disease (CKD) can have a considerable impact on the lives of children and young people (CYP) with the disease and those of their families.1–3 Impaired physical growth and difficulties of psychosocial adjustment can impair quality of life, with some CYP experiencing depression and adjustment disorders.4 Professionals working with CYP with CKD recognise these can report difficulties with low mood, anxiety, body image, friendships, schooling, loneliness, isolation, pain and fatigue, as well as existential thoughts of ‘Why me?’.

A 21-year-old male Caucasian patient presented as an emergency with end-stage renal disease (ESRD), with a creatinine concentration of 2,852 µmol/l, features of chronic nephritis with proteinuria (urine protein:creatinine ratio of 407.4 mg/mmol), and atrophic kidneys on ultrasonography. Investigations for Fabry disease (alpha-galactosidase A), HIV and hepatitis B/C infection and immune-mediated renal disease (antinuclear, antineutrophil cytoplasmic and anti-glomerular basement membrane antibodies) were all negative. The patient was commenced on renal replacement therapy (RRT), initially in the form of haemodialysis (HD) and subsequently switched to peritoneal dialysis (PD). As PD was unsuccessful because of inadequate dialysis, he was switched back on to HD and was evaluated for a living donor transplant. At initial presentation, he was commenced on the H2 receptor antagonist ranitidine, administered orally at a dose of 150 mg twice a day. This was prompted by concerns about his severe anaemia (haemoglobin <40 g/l) and high risk of peptic ulceration in the setting of an extreme uraemic emergency.

People with kidney disease have been hugely affected by the pandemic. Those with kidney transplants and receiving immunosuppressive drugs to control their kidney disease were contacted and advised to self-isolate for at least 12 weeks at the start of the pandemic. They became part of the 2.2 million people in England who have been shielding over these past three months. It became apparent early on that, alongside other risk multipliers of age and being part of a BAME community, people receiving maintenance haemodialysis had a high risk of infection and mortality and, as such, were advised to shield, other than their necessary visits to the haemodialysis unit. In a number of units haemodialysis was reduced from three times per week to twice weekly for those patients able to tolerate this reduction. Control of potassium was made possible by the use of the newer potassium binding agents for these patients.

A cute kidney injury (AKI) is the loss of kidney function over a short period of time and manifests as a rise in serum creatinine levels from baseline and/or a fall in urine output. It is well established that AKI is associated with high rates of mortality and morbidity and it has been estimated that 1.7 million deaths worldwide are attributable to AKI annually. The burden of AKI disproportionally affects low- and middle-income countries (LMICs), where the resources are most scarce.

BK virus (BKV) reactivation following kidney transplantation is estimated to occur in up to 10% of recipients and can cause the development of an associated nephropathy. BKV nephropathy results in long-term allograft damage, a reduction in graft longevity and graft loss in 15–50% of those affected.1 Transplants may also be lost due to rejection, triggered by a reduction in immunosuppression aimed at preventing BKV replication. Risk factors for BKV nephropathy are not fully understood, but intensity of immunosuppression and certain donor and recipient characteristics are known to contribute to the risk.