Acute kidney injury (AKI) is a complex disorder for which currently there is no accepted definition. Having a uniform standard for diagnosing and classifying AKI would enhance our ability to manage these patients. Future clinical and translational research in AKI will require collaborative networks of investigators drawn from various disciplines, dissemination of information via multidisciplinary joint conferences and publications, and improved translation of knowledge from pre-clinical research. We describe an initiative to develop uniform standards for defining and classifying AKI and to establish a forum for multidisciplinary interaction to improve care for patients with or at risk for AKI. Members representing key societies in critical care and nephrology along with additional experts in adult and pediatric AKI participated in a two day conference in Amsterdam, The Netherlands, in September 2005 and were assigned to one of three workgroups. Each group's discussions formed the basis for draft recommendations that were later refined and improved during discussion with the larger group. Dissenting opinions were also noted. The final draft recommendations were circulated to all participants and subsequently agreed upon as the consensus recommendations for this report. Participating societies endorsed the recommendations and agreed to help disseminate the results. The term AKI is proposed to represent the entire spectrum of acute renal failure. Diagnostic criteria for AKI are proposed based on acute alterations in serum creatinine or urine output. A staging system for AKI which reflects quantitative changes in serum creatinine and urine output has been developed. We describe the formation of a multidisciplinary collaborative network focused on AKI. We have proposed uniform standards for diagnosing and classifying AKI which will need to be validated in future studies. The Acute Kidney Injury Network offers a mechanism for proceeding with efforts to improve patient outcomes.

Acute Kidney Injury Network: report of an initiative to improve outcomes in acute kidney injury

Vascular calcification (VC), which is categorized by intimal and medial calcification, depending on the site(s) involved within the vessel, is closely related to cardiovascular disease. Specifically, medial calcification is prevalent in certain medical situations, including chronic kidney disease and diabetes. The past few decades have seen extensive research into VC, revealing that the mechanism of VC is not merely a consequence of a high-phosphorous and -calcium milieu, but also occurs via delicate and well-organized biologic processes, including an imbalance between osteochondrogenic signaling and anticalcific events. In addition to traditionally established osteogenic signaling, dysfunctional calcium homeostasis is prerequisite in the development of VC. Moreover, loss of defensive mechanisms, by microorganelle dysfunction, including hyper-fragmented mitochondria, mitochondrial oxidative stress, defective autophagy or mitophagy, and endoplasmic reticulum (ER) stress, may all contribute to VC. To facilitate the understanding of vascular calcification, across any number of bioscientific disciplines, we provide this review of a detailed updated molecular mechanism of VC. This encompasses a vascular smooth muscle phenotypic of osteogenic differentiation, and multiple signaling pathways of VC induction, including the roles of inflammation and cellular microorganelle genesis.

Vascular Calcification-New Insights Into Its Mechanism.

Sjogren's syndrome: An update on disease pathogenesis, clinical manifestations and treatment.

An ideal tool for all radiology residents and students, it covers all subspecialty areas and current imaging modalities as utilized in neuroradiology, chest, breast, abdominal, musculoskeletal imaging, ultrasound, pediatric imaging, interventional techniques and nuclear radiology. New and expanded topics in this edition include use of diffustion-weighted MR, new contrast agents, breast MR, and current guidelines for biopsy and intervention. Many new images, expanded content, and full-color throughout make the fourth edition of this classic text a comprehensive review that is ideal as a first reader for beginning residents, a reference during rotations, and a vital resource when preparing for the American Board of Radiology examinations.

Fundamentals of Diagnostic Radiology

https://cyberleninka.org/article/n/675468.pdf

Serum uric acid and acute kidney injury: A mini review

Cyst infection is a common complication of autosomal dominant polycystic kidney disease. It presents with vague clinical features and imaging findings which make the diagnosis challenging. Imaging findings can be misinterpreted as renal cell carcinoma, and biopsy of the lesion is often required for definitive diagnosis.

https://www.onlinelibrary.wiley.com/doi/pdf/10.1002/ccr3.1441

Renal cyst infection: a diagnostic dilemma.

https://www.ajkd.org/article/S0272-6386(20)31015-5/pdf

Use of Point-of-Care Ultrasound to Assess CKD.

The mean age of onset of end-stage renal disease (ESRD) in autosomal dominant polycystic kidney disease (ADPKD) is between 56 and 69. Our case represents one of the oldest patients with ADPKD, whose chronic kidney disease (CKD) progression rate could be successfully reduced by optimal risk factor modification.

An 88-year-old patient with ADPKD: underscoring the importance of risk factor modification

To the Editor Recently, it has been shown that acute kidney injury (AKI) is a risk factor for the development of subsequent proteinuria, which in turn could predispose to chronic kidney disease (CKD) [1]. Interestingly, this association persisted regardless of the diabetes status and the use of ACEI/ARB at baseline. As we know, prior AKI episodes and proteinuria have both been implicated in progressive CKD, but the precise underlying mechanisms remain elusive. In our opinion, the missing link could be the loss of renal functional reserve (RFR) after an episode of AKI. Though described more than 30 years ago, RFR largely remains an underexplored concept. RFR is defined as the difference between ‘stress’ GFR and ‘baseline’ GFR, where stress GFR represents the supranormal GFR clinically elicited by intake of a protein load (Fig. 1a). In other words, RFR is the reserve capacity of the kidney to increase GFR in response to physiologic or pathologic stimuli. Even with up to 50% of the functional renal tissue damaged during an episode of AKI, hyperfiltration in the remaining nephrons would compensate for the lost function, keeping serum creatinine value near baseline (Fig. 1b, c) [2, 3]. On the other hand, glomerular hyperfiltration has been linked to the development of albuminuria, as typically seen in those with diabetes and solitary kidney [4, 5]. As such, we propose that the loss of RFR after AKI could lead to hyperfiltration-associated proteinuria. Future studies are needed to explore whether measurement of RFR after the clinical recovery of AKI may help stratify the risk of proteinuria and CKD. More experimental data are required to elucidate other potential mechanisms underlying the RFR in addition to hyperfiltration, especially in non-proteinuric CKD.

Reduced renal functional reserve as the mechanism linking acute kidney injury to proteinuria.

Abstract is not required for Clinical Imagesis not required for Clinical Images (This page in not part of the published article.) International Journal of Case Reports and Images, Vol. 8 No. 2, February 2017. ISSN – [0976-3198] Int J Case Rep Images 2017;8(2):165–167. www.ijcasereportsandimages.com Bhatti et al. 165 CASE REPORT OPEN ACCESS Renal cell carcinoma of the native kidney in a renal transplant recipient Vikrampal Bhatti, Ananthalaxmi Vangapalli, Deepti Bhattacharya, Abhilash Koratala

/pdf/renal-cell-carcinoma-of-the-native-kidney-in-a-renal-53db58eftj.pdf

Abhilash Koratala

Papers

Renal cyst infection: a diagnostic dilemma.

Use of Point-of-Care Ultrasound to Assess CKD.

An 88-year-old patient with ADPKD: underscoring the importance of risk factor modification

Reduced renal functional reserve as the mechanism linking acute kidney injury to proteinuria.

Renal cell carcinoma of the native kidney in a renal transplant recipient