Pharmacological Nephroprotection in Non-Diabetic Chronic Kidney Disease-Clinical Practice Position Statement of the Polish Society of Nephrology

J Clin Med. 2023 Aug 9;12(16):5184. doi: 10.3390/jcm12165184.


Chronic kidney disease (CKD) is a modern epidemic worldwide. Introducing renin-angiotensin system (RAS) inhibitors (i.e., ACEi or ARB) not only as blood-pressure-lowering agents, but also as nephroprotective drugs with antiproteinuric potential was a milestone in the therapy of CKD. For decades, this treatment remained the only proven strategy to slow down CKD progression. This situation changed some years ago primarily due to the introduction of drugs designed to treat diabetes that turned into nephroprotective strategies not only in diabetic kidney disease, but also in CKD unrelated to diabetes. In addition, several drugs emerged that precisely target the pathogenetic mechanisms of particular kidney diseases. Finally, the role of metabolic acidosis in CKD progression (and not only the sequelae of CKD) came to light. In this review, we aim to comprehensively discuss all relevant therapies that slow down the progression of non-diabetic kidney disease, including the lowering of blood pressure, through the nephroprotective effects of ACEi/ARB and spironolactone independent from BP lowering, as well as the role of sodium-glucose co-transporter type 2 inhibitors, acidosis correction and disease-specific treatment strategies. We also briefly address the therapies that attempt to slow down the progression of CKD, which did not confirm this effect. We are convinced that our in-depth review with practical statements on multiple aspects of treatment offered to non-diabetic CKD fills the existing gap in the available literature. We believe that it may help clinicians who take care of CKD patients in their practice. Finally, we propose the strategy that should be implemented in most non-diabetic CKD patients to prevent disease progression.

Keywords: Fabry disease; angiotensin II receptor blockers; angiotensin-converting enzyme inhibitors; autosomal-dominant polycystic kidney disease; blood pressure control; chronic kidney disease; metabolic acidosis; renin–angiotensin system; sodium–glucose co-transporter type 2 inhibitors.

Publication types

  • Review

Grants and funding

This statement received no external funding (except for publication costs covered by the Polish Society of Nephrology).