Background And Purpose: The management of polycystic kidney disease is mostly restricted to conservative measures. However, nephrectomy may be indicated in particular cases, especially when there are infective complications. To decrease the morbidity of the procedure, the laparoscopic approach has become appealing. We present a laparoscopic retroperitoneal approach to complicated polycystic kidney disease in a high-risk patient. CASERESPORT: We performed right retroperitoneal laparoscopic nephrectomy in a 39-year-old man who had autosomal polycystic kidney disease and had undergone heart transplantation. The immunosuppressed patient presented with severe flank pain, generalized signs of infection, and acute renal insufficiency. With the patient in the right lateral decubitus position, the retroperitoneal space was entered by the open technique, and the posterior pararenal space was developed with finger dissection. Five trocars were used. After the renal vessels had been secured and divided, the cysts were successively punctured, gradually shrinking the operative specimen. The kidney was placed in an Endo-catch and removed after morcellation, with no need to enlarge the 2-cm lumbotomy. The operating time was 80 minutes, and the hospital stay was 4 days. Histologic examination revealed a polycystic kidney with Aspergillus infection.
Conclusion: The laparoscopic approach is a less-invasive option for removing a polycystic kidney when nephrectomy is indicated. The retroperitoneal route has the advantage of minimizing infection risks because of the absence of peritoneal opening.
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http://dx.doi.org/10.1089/089277902753752205 | DOI Listing |
Bone Res
January 2025
Department of Endocrinology, Endocrinology Research Center, Xiangya Hospital of Central South University, Changsha, Hunan, 410008, China.
Mechanical stress modulates bone formation and organization of the extracellular matrix (ECM), the interaction of which affects heterotopic ossification (HO). However, the mechanically sensitive cell populations in HO and the underlying mechanism remain elusive. Here, we show that the mechanical protein Polysyctin-1 (PC1, Pkd1) regulates CTSK lineage tendon-derived mesenchymal stem cell (TDMSC) fate and ECM organization, thus affecting HO progression.
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Department of Paediatric Nephrology, The Royal Children's Hospital, Melbourne, Australia.
Hepatopulmonary syndrome (HPS) is a life-threatening complication of chronic liver disease (CLD) that currently can be managed only by liver transplant. Though uncommon, some children with kidney disease have coexistent CLD and hence are at risk of developing HPS. Paediatric cases of HPS are rarely described in the nephrology literature.
View Article and Find Full Text PDFHeart Lung Circ
January 2025
Department of Cardiovascular Surgery, Shizuoka Medical Center, Shizuoka, Japan. Electronic address:
Prog Mol Biol Transl Sci
January 2025
Department of Pharmacy, Birla Institute of Technology and Science Pilani, Pilani Campus, Rajasthan, India. Electronic address:
Recent advances in CRISPR-Cas systems have revolutionised the study and treatment of kidney diseases, including acute kidney injury (AKI), chronic kidney disease (CKD), diabetic kidney disease (DKD), lupus nephritis (LN), and polycystic kidney disease (PKD). CRISPR-Cas technology offers precise and versatile tools for genetic modification in monogenic kidney disorders such as PKD and Alport syndrome. Recent advances in CRISPR technology have also shown promise in addressing other kidney diseases like AKI, CKD, and DKD.
View Article and Find Full Text PDFPhysiol Rep
January 2025
Developmental Biology and Cancer Research and Teaching Department, University College London, Great Ormond Street Institute of Child Health, London, UK.
Polycystic kidney diseases (PKD) are genetic disorders which disrupt kidney architecture and function. Autosomal recessive PKD (ARPKD) is a rare form of PKD, caused by mutations in PKHD1, and clinically more severe than the more common autosomal dominant PKD (ADPKD). Prior studies have implicated Hedgehog (Hh) signaling in ADPKD, with increased levels of Hh components in experimental ADPKD and reduced cystogenesis following pharmacological Hh inhibition.
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