1.
Kidney injury and disease in patients with haematological malignancies.
Bridoux, F, Cockwell, P, Glezerman, I, Gutgarts, V, Hogan, JJ, Jhaveri, KD, Joly, F, Nasr, SH, Sawinski, D, Leung, N
Nature reviews. Nephrology. 2021;(6):386-401
Abstract
Acute kidney injury (AKI) is common in patients with cancer, especially in those with haematological malignancies. Kidney injury might be a direct consequence of the underlying haematological condition. For example, in the case of lymphoma infiltration or extramedullary haematopoiesis, it might be caused by a tumour product; in the case of cast nephropathy it might be due to the presence of monoclonal immunoglobulin; or it might result from tumour complications, such as hypercalcaemia. Kidney injury might also be caused by cancer treatment, as many chemotherapeutic agents are nephrotoxic. High-intensity treatments, such as high-dose chemotherapy followed by haematopoietic stem cell transplantation, not only increase the risk of infection but can also cause AKI through various mechanisms, including viral nephropathies, engraftment syndrome and sinusoidal obstruction syndrome. Some conditions, such as thrombotic microangiopathy, might also result directly from the haematological condition or the treatment. Novel immunotherapies, such as immune checkpoint inhibitors and chimeric antigen receptor T cell therapy, can also be nephrotoxic. As new therapies for haematological malignancies with increased anti-tumour efficacy and reduced toxicity are developed, the number of patients receiving these treatments will increase. Clinicians must gain a good understanding of the different mechanisms of kidney injury associated with cancer to better care for these patients.
2.
Dengue hemorrhagic fever and the kidney.
Vachvanichsanong, P, Thisyakorn, U, Thisyakorn, C
Archives of virology. 2016;(4):771-8
Abstract
Dengue virus infection (DVI)/dengue hemorrhagic fever (DHF) is a common febrile illness with a variety of severities. The mortality rate is high in dengue shock syndrome (DSS), caused by circulatory failure due to plasma leakage resulting in multi-organ failure. However, acute kidney injury (AKI) is rarely reported. In areas of endemic DVI, the prevalence of AKI due to DVI has been reported to be as high as 6.0 % in children with AKI, and 0.9 % in children with DVI who were admitted to a hospital. The mechanism of AKI in DVI is not clear. It may result from (a) direct injury as in other infectious diseases, (b) an indirect mechanism such as via the immune system, since DHF is an immunological disease, or (c) hypotensive DSS, leading in turn to reduced renal blood supply and renal failure. The mortality rates of DF/DHF, DSS and DHF/DSS-related AKI are <1 %, 12-44 %, and >60 %, respectively. Kidney involvement is not actually that rare, but is under-recognized and often only reported when microscopic hematuria, proteinuria, electrolyte imbalance, or even AKI is found. The prevalence of proteinuria and hematuria has been reported as high as 70-80 % in DVI. A correct diagnosis depends on basic investigations of kidney function such as urinalysis, serum creatinine and electrolytes. Although DVI-related renal involvement is treated supportively, it is still important to make an early diagnosis to prevent AKI and its complications, and if AKI does occur, dialysis may be required. Fortunately, in patients who recover, kidney function usually completely recovers as well.
3.
Removal characteristics and total dialysate content of glutamine and other amino acids in critically ill patients with acute kidney injury undergoing extended dialysis.
Schmidt, JJ, Hafer, C, Spielmann, J, Hadem, J, Schönenberger, E, Schmidt, BM, Kielstein, JT
Nephron. Clinical practice. 2014;(1):62-6
Abstract
BACKGROUND Acute kidney injury in critically ill patients is associated with the activation of protein catabolism and a negative nitrogen balance. Renal replacement therapy (RRT) aggravates this problem by eliminating a substantial amount of amino acids. However, there is scarce data on the removal characteristics of modern dialysis membranes in extended dialysis. METHODS This is a prospective study in 10 extended dialysis sessions using a 1.8-m(2) polysulfone membrane (EMiC2 dialyzer or AV 1000S; FMC, Germany). Blood samples for 19 amino acids were drawn before, during, and after 10 h of extended dialysis (blood/dialysate flow 150 ml/min). In addition, samples for the calculation of dialyzer clearance and samples from the total spent dialysate were measured using a Biochrom 30 amino acid analyzer. RESULTS Despite no significant difference in pre- and postdialysis plasma amino acid levels, we found an impressive amount of amino acids in collected spent dialysate, i.e. 10.5 g/10 h of treatment. The dialyzer clearance ranged from 67.6 ml/min for phenylalanine to 140.0 ml/min for valine. The total eliminated masses of the measured amino acids had equal values for both membranes. There was a significant difference between the dialyzer clearance of the investigated membranes for glutamine (AV 1000S: 83.3 ml/min vs. EMiC2: 92.0 ml/min, p = 0.02) and serine (88.8 ml/min vs. 91.8 ml/min, p = 0.005). DISCUSSION Our data indicate that the modern forms of RRT eliminate amino acids to an extent that has not been met by our nutritional support standards. Especially the removal of glutamine, important for immune function and cell regeneration, might have detrimental effects on the recovery of critically ill patients.
4.
Acute and chronic kidney injury in nephrolithiasis.
Tang, X, Lieske, JC
Current opinion in nephrology and hypertension. 2014;(4):385-90
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Abstract
PURPOSE OF REVIEW Nephrolithiasis is a common systemic disease associated with both acute kidney injury (AKI) and chronic kidney disease (CKD). The purpose of this review is to discuss recent publications regarding nephrolithiasis-associated kidney damage, with an emphasis on AKI. RECENT FINDINGS Nephrolithiasis is not a common cause of adult AKI (1-2% of cases), although it may be a more important factor in young children (up to 30%). The primary mechanism of nephrolithiasis-associated AKI is obstructive nephropathy, and factors on presentation with obstructive uropathy predict the likelihood of long-term renal recovery. Crystalline nephropathy is another potential pathway in certain circumstances that is often associated with a worse outcome. Recent studies have elucidated additional pathways whereby calcium oxalate crystals can cause acute injury, implicating innate immunity and intracellular inflammasome pathways. Several large cohort studies have demonstrated an independent association of nephrolithiasis with CKD and end-stage renal disease, although the effect size is modest. Urologic comorbidities, urinary infection, and shared underlying risk factors (e.g., diabetes, hypertension) all impact nephrolithiasis-associated CKD risk. SUMMARY Obstructive nephropathy and crystalline nephropathy both contribute to nephrolithiasis-associated AKI, although the latter appears to have a worse prognosis. Nephrolithiasis is an independent, albeit small, risk factor for CKD. Further study is needed to clarify the incidence and mechanisms of nephrolithiasis-associated AKI, and the relationship between nephrolithiasis-associated AKI and CKD.