Acute kidney injury (AKI) is one of the most dangerous complications in intensive care units, affecting up to half of critically ill patients and sharply increasing mortality risk. A common but preventable contributor to AKI is cast nephropathy, in which obstructive protein or pigment casts form inside kidney tubules. This condition is frequently missed because standard indicators such as serum creatinine and urine output rise only after significant damage has occurred. Now, a new narrative review shows that earlier detection and targeted intervention could substantially improve kidney recovery and survival.

The review by researchers from the University of Trento (Trento, Italy) focused on cast nephropathy as an under-recognized cause of AKI in critically ill patients. Cast nephropathy arises when circulating substances such as free light chains, myoglobin, bilirubin, or hemoglobin precipitate within renal tubules. These casts obstruct flow and trigger oxidative stress, inflammation, and tubular injury. Because a kidney biopsy is often unsafe in unstable ICU patients, diagnosis usually relies on indirect signs. Conventional laboratory tests detect injury late, when scarring and functional loss may already be established.

The review, published in the Journal of Intensive Medicine, highlights the need for diagnostic strategies that identify tubular stress before irreversible damage occurs. The authors emphasize the growing clinical value of novel biomarkers such as NGAL, cystatin C, and the cell-cycle arrest markers TIMP-2 and IGFBP7. These biomarkers can detect early tubular stress hours or days before changes in creatinine or urine output. Their use could allow clinicians to intervene while kidney injury is still potentially reversible.

The review also shows that cast nephropathy is biologically heterogeneous. The molecule responsible for cast formation determines both disease severity and optimal treatment approach. This variability helps explain why uniform treatment strategies have produced inconsistent outcomes. A central conclusion of the review is that extracorporeal blood purification therapies should be tailored to the causative molecule rather than applied uniformly. Techniques such as high-cutoff membranes, adsorption devices, or plasma exchange may be effective when matched to the specific pathogenic protein or pigment.

These approaches are most beneficial when combined with disease-directed therapy, such as chemotherapy for multiple myeloma or complement inhibition for hemolytic disorders. Going forward, the authors describe a future role for artificial intelligence (AI) systems that integrate biomarkers, laboratory data, and imaging to identify cast-related AKI before clinical deterioration. Such tools could shift extracorporeal therapies from late rescue interventions to proactive kidney-protective strategies.

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