Background/Objectives: Lupus nephritis (LN) is one of the most severe organ manifestations of systemic lupus erythematosus (SLE). Chronic kidney disease (CKD) and its progression into end-stage renal disease (ESRD) are serious complications in LN and the main cause of death in SLE. We aimed to investigate the prognostic factors of the progression of CKD and the development of ESRD in SLE patients. Methods: In our retrospective cohort study, we assessed the clinical and laboratory data of 127 patients who were diagnosed with LN between 1990 and 2022 and received regular follow-up care at our autoimmune centre. We compared class IV (diffuse) LN patients with non-class IV LN patients and assessed the differences in clinical and laboratory data of the patients, subdivided into complete, partial, and non-responders to therapy. Results: The prevalence of class IV LN is significantly higher in patients with CKD stage 3–5. Age above 42, class IV LN, Coombs positivity, and high chronicity index are prognostic factors for the development of CKD stage 3–5. On the other hand, anti-RNP and anti-SS-B antibody positivity and a high chronicity index are prognostic factors for the development of ESRD. The chronicity index, as well as the SLICC/ACR Damage Index (SDI) score, was significantly higher in non-responders compared to patients with complete remission. Conclusions: Based on our results, the progression of CKD into stage 3–5 or the development of ESRD should be expected at a chronicity index above 3.5 points. An early diagnosis, as well as aggressive, timely, and adequate treatment, is fundamental to prevent unfavourable outcomes of LN.

In light chain amyloidosis (LA), the massive glomerular and vascular amyloid deposition leading to interstitial fibrosis/tubular atrophy (IFTA) is thought to be responsible for renal failure. The amyloid deposition in the interstitium and the tubular basement membrane (TBM) has received less attention in the study of LA. We, therefore, collected clinical and laboratory data on patients diagnosed with LA in our Nephrology Department and studied amyloid deposition in the TBM. Twelve LA patients were diagnosed by renal biopsy during a seven-year period. In 4 of the 12, amyloid deposition could also be detected in the TBM. In our first case of a patient with diabetes mellitus, non-amyloid fibrils resembling ‘diabetic fibrillosis’ were also seen by electron microscopy. Despite the double damage, IFTA was negligible, blood vessels were unaffected, and the glomerular deposition was segmental. In the other three cases, significant (>50%) IFTA and a severely reduced estimated glomerular filtration rate were already detected at the time of diagnosis and amyloid deposition was also observed in the blood vessels. These findings indicate the importance of TBM amyloid deposition in the progression of renal disease. This may represent a late-stage presentation of the disease with a heavy LC burden.