Osmotic Nephropathy Induced by L-Proline Stabilized Sucrose-free Intravenous Immunoglobulins: A Case Report

Sep 29, 2026

Acute kidney injury after sucrose-free intravenous immunoglobulins (IVIG) is uncommon. This case report describes a 67-year-old man with Guillain-Barré syndrome who developed sudden anuric acute kidney injury on day 4 after L-proline stabilized sucrose-free IVIG. IVIG was stopped, no renal replacement therapy was needed, and renal function fully recovered within two weeks. Kidney biopsy showed osmotic nephropathy, without ischemic acute tubular necrosis, glomerular/vascular involvement, or antibody deposition. The authors propose that proline acted as a toxic solute accumulating in lysosomes, leading to osmotic nephropathy.

LanguageEnglish

CategoryHealthcare

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Reading Time13 min

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Case Report

Patient presentation and clinical course

Diagnostic evaluation and biopsy findings

Proposed mechanisms and discussion

Case Report Osmotic Nephropathy Induced by L-Proline Stabilized Sucrose-free Intravenous Immunoglobulins: A Case Report Antonio Ulpiano Trillig, Samuel Rotman, Patricia Mehier, Alain Rossier, and Grard Vogel Acute kidney injury following sucrose-free intravenous immunoglobulins (IVIG) is rare. We report the case of a 67-year-old male who developed a sudden anuric acute kidney injury at day 4 of L-proline stabilized sucrose-free IVIG for a Guillain-Barr Syndrome. The IVIG treatment was halted. The patient did not require renal replacement therapy after an adequate response to diuretics. Amoxicillin was the sole other potential nephrotoxic. The kidney biopsy showed typical features of osmotic nephropathy (ON) . Although a certain degree of kidney hypoxia due to dysautonomia and variations of blood pressure might have occurred, histological findings were not compatible with an ischemic acute tubular necrosis. There was no glomerular and vascular involvement. Immunofluorescence of tubular cells cytoplasm was negative, ruling out antibody deposition. The patient had a complete renal recovery after 2 weeks. We hypothesize that proline itself acted as a reabsorbed toxic solute and accumulated in the lysosomes, leading to ON. In this case report we discuss the proline proximal tubular transport, involving pinocytosis in case of high concentration in the filtrate, and potential mechanisms involved in the development of ON. Complete author and article information provided before references. Correspondence to A. Ulpiano Trillig (antonio. ulpiano-trillig@chuv.ch) Kidney Med. 8(1):101172. Published online November 4, 2025. doi: 10.1016/j. xkme.2025.101172 © 2025 The Authors. Published by Elsevier Inc. on behalf of the National Kidney Foundation, Inc. This is an open access article under the CC BY license ([http://creativecommons.org/licenses/by/4.0/](http://creativecommons.org/licenses/by/4.0/)). Acute IVIG kidney injury (AKI) following administration of is well described with the use of sucrose con- taining IVIG. 1 It is thought to be triggered by the proximal tubule reabsorption of a large amount of sucrose, notably by pinocytosis, with pinocytic vacuoles fusing with lysosomes. 1 , 2 The accumulation of lysosomes in tubular cells, favored in the setting of altered lysosomal digestion such asa hypoxic state, leads to cellular dysfunction and swelling, lysosomal rupture, and ultimately AKI. 1-3 A certain degree of tubular obstruction due to swelling of the tubular epithelium is possible.2 On electronic microscopy, atypical feature of this condition is lysosomal vacuoles containing amorphous debris.2 ,4 This process is termed osmotic nephropathy in the literature, although no osmotic effect is involved. 1 , 5 It is described with the infusion of different agents such as mannitol, sorbitol, hydroxyethyl starch, contrast medium, and more recently with SGLT2 inhibitors, possibly involving glucose reabsorption in S3 segment of proximal tubule by pinocytosis. 1 , 2 ,4 , 5 L-proline stabilized IVIG are very rarely associated with AKI. After administration of such IVIG, AKI is only described in the setting of hemoglobinuria and hemolytic anemia,6 , 7 but to our knowledge no case of osmotic nephropathy (ON) was previously reported. We describe the case of an anuric AKI with biopsyproven ON following L-proline stabilized sucrose-free IVIG perfusion. Case Report A 67-year-old male with a medical history of treated arterial hypertension was admitted to the intensive care unit for an acute inflammatory demyelinating polyneuropathy following a SARS-CoV-2 infection. The infection began 17 days before his admission, with mild upper respiratory symptoms and a dry cough, already resolved on admission. There was no indication for remdesivir nor any SARS-CoV-2 infection specific treatment. He was tetraparetic and presented wide variations of blood pressure due to dysautonomia, requiring intermittent use of intravenous nic

FAQs

What treatment triggered the acute kidney injury in this case?

The patient received L-proline stabilized sucrose-free IVIG for Guillain-Barré syndrome, and the anuric AKI occurred on day 4 after initiation.

What did the kidney biopsy show?

The biopsy demonstrated typical features of osmotic nephropathy, with findings not compatible with ischemic acute tubular necrosis and without glomerular or vascular involvement.

How did the patient’s kidney function progress after stopping IVIG?

IVIG was halted and diuretics were used; the patient achieved complete renal recovery after two weeks without requiring renal replacement therapy.

Sep 29, 2026

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