Rheumatology and the kidney connection

Attendees at the Irish Society for Rheumatology Spring Meeting 2023 heard from Dr Brenda Griffin, Consultant Nephrologist at St James’s Hospital in Dublin, whose talk was titled, ‘What rheumatologists need to know about the kidneys’. Dr Griffin presented a number of case studies on patients with Sjogren’s syndrome and systemic sclerosis. 

“In primary Sjogren’s syndrome of the kidney, the prevalence is quoted as between 1 and 33 per cent,” said Dr Griffin. “But if you’re a nephrologist working in a big centre with a big rheumatology department like St James’s Hospital, it seems like almost all of the patients [have renal involvement]. One hundred per cent of my Sjogren’s patients also have renal involvement.” Dr Griffin said some conditions are reasonably homogenous, but in Sjogren’s syndrome, it is heterogenous, with different types of pathology. “Chronic tubulointerstitial nephritis is the most common, but then there are the tubular abnormalities,” she told the conference. “You can get proximal and distal renal tubular acidosis, nephrogenic diabetes insipidus, low potassium and Gitelman syndrome with it, and there is also glomerular disease, proliferative glomerular nephritis, and with hypercalciuria, you can get microlithiasis.”

Dr Griffin also discussed the importance of the acid-base balance: “The renal handling of acid-base is two phenomena,” she told the meeting. “In the proximal tubule, we reabsorb bicarbonate, and in the distal convoluted tubule and the collecting duct, we produce hydrogen ions… the sodium chloride co-transporter is in the distal collecting duct, and that’s where thiazide diuretics work. So essentially, you don’t reabsorb sodium and you get diuresis.”

She described how in the proximal tubule, there is a promiscuous hydrogen ion that escorts bicarbonate from the urinary space and back to the capillary space, and she gave the conference an overview of this process. “With distal renal tubular acidosis in primary Sjogren’s syndrome, you have complete absence of the hydrogen atpA; that’s distal and that’s how we dispose of hydrogen ions. But you can also have autoantibodies against carbonic anhydrides too, and that will stop you reabsorbing bicarbonate in the proximal tubules.” 

She described Gitelman’s syndrome as a sodium-wasting condition and in classical Gitelman’s, there is an abnormality in the gene SLC12a3, which is the gene encoding the sodium chloride transporter, which is thiazide-sensitive. “So really, you are not reabsorbing sodium in this condition, it is sodium-wasting and that extra sodium delivery to the collecting duct causes volume depletion, and it enhances the release of aldosterone because of the volume depletion,” Dr Griffin told the attendees. “That means you are not able to exchange sodium and potassium and you get hypokalaemia, hypomagnesaemia, hypercalciuria, and alkalosis and even though you get secondary hyperaldosteronism, it’s kind of volume depletion versus secondary hyperaldosteronism, but, generally, the patient is not hypertensive.”