Submitted Successfully!
To reward your contribution, here is a gift for you: A free trial for our video production service.
Thank you for your contribution! You can also upload a video entry or images related to this topic.
Version Summary Created by Modification Content Size Created at Operation
1
Peter Schnuelle
 -- 2120 2023-10-31 19:25:38 |
2 layout
Sirius Huang
 Meta information modification 2120 2023-11-06 02:15:25 |

Video Upload Options

Do you have a full video?
Send video materials Upload full video

Confirm

Are you sure to Delete?
Yes No
Cite
If you have any further questions, please contact Encyclopedia Editorial Office.
Schnuelle, P. Indication for Renal Biopsy. Encyclopedia. Available online: https://encyclopedia.pub/entry/51011 (accessed on 31 July 2024).
Schnuelle P. Indication for Renal Biopsy. Encyclopedia. Available at: https://encyclopedia.pub/entry/51011. Accessed July 31, 2024.
Schnuelle, Peter. "Indication for Renal Biopsy" Encyclopedia, https://encyclopedia.pub/entry/51011 (accessed July 31, 2024).
Schnuelle, P. (2023, October 31). Indication for Renal Biopsy. In Encyclopedia. https://encyclopedia.pub/entry/51011
Schnuelle, Peter. "Indication for Renal Biopsy." Encyclopedia. Web. 31 October, 2023.
Indication for Renal Biopsy
Edit
This entry is adapted from the peer-reviewed paper 10.3390/jcm12196424

Acute and progressive chronic kidney diseases are subject to a variety of inflammatory and autoimmune processes, which are often accompanied by degenerative lesions or are also genetically determined. Renal biopsies are the gold standard for diagnosis, staging, and prognosis of underlying parenchymal kidney disease.

renal biopsy indication clotting disorder hypertension real-time ultrasound spring-loaded biopsy device biopsy needle size bleeding laparoscopic-assisted biopsy transjugular renal biopsy

1. Introduction

Acute and progressive chronic kidney diseases are subject to a variety of inflammatory and autoimmune processes, which are often accompanied by degenerative lesions or are also genetically determined. In many cases, the underlying causes cannot be distinguished clinically, nor can they be identified by advanced laboratory tests because they remain confined to the renal parenchyma. Therefore, a renal biopsy is indicated when knowledge of the histological diagnosis is essential for appropriate therapy [1][2]. Nevertheless, there is general agreement that the biopsy findings should always be viewed and interpreted in the context of clinical and historical data. In addition to histological diagnosis, a renal biopsy also allows the prognosis of underlying renal disease to be assessed. However, the advantages of histological diagnosis must always be weighed against the possible risks due to the invasive nature of the procedure [3][4]. For optimization of the diagnostic significance, the biopsy sample should routinely be subjected to light microscopy, immunofluorescence, and electron microscopy [5][6][7]. Additional new modern pathology techniques based on gene expression analysis and proteomics, in situ detection of functionally relevant molecules, and new bioinformatics approaches have the potential to provide deep insights into the mechanisms behind the morphological findings and refine molecular pathways for treatment interventions [8][9]. A recent example of this is severe acute respiratory syndrome coronavirus type 2 (SARS-CoV-2) associated nephropathy. SARS-CoV-2-associated nephropathy, in particular, has been extensively characterized through the application of state-of-the-art molecular pathological methods. Both the receptor protein (angiotensin-converting enzyme 2 [ACE-2] receptor) and the virus itself have been visualized in tubular cells using fluorescence in situ hybridization [10][11]. Acute tubular injury is the most common renal involvement in patients infected with SARS-CoV-2, followed by thrombotic microangiopathy (TMA) and necrotizing glomerulonephritis, establishing SARS-CoV-2-nephropathy as a distinct entity.
The available evidence suggests that the histological diagnosis of both native and transplanted kidney biopsies has a direct therapeutic impact or significantly influences the patient’s further treatment in about 40–60% of cases [12][13]. Apart from protocol biopsies for scientific purposes, the indication for performing a renal biopsy is determined in individual cases by the subjective assessment of the treating nephrologist with regard to the therapeutic benefit [14][15]. There are considerable differences in the indication and performance of a kidney biopsy locally in the nephrology departments and also in an international comparison [16][17]. Comparing the biopsy frequency in Australia and in the USA on the basis of a cross-sectional survey from 1995 to 1997 revealed that more than 250 kidney biopsies per million population were performed in Australia, while this figure was less than 75 per million population in the USA [18].

2. Indications

Table 1 summarizes the current indications for native and transplant kidney biopsies. Classic indications for biopsy of the patient’s own kidney include new-onset nephrotic syndrome in adults, evidence of proteinuria greater than 1–2 g/24 h with or without hypertension, and impaired renal function of unknown cause, especially when an active urine sediment indicates possible crescentic glomerulonephritis. Furthermore, if renal involvement is suspected in association with an immunological or paraneoplastic systemic disease, e.g., antineutrophil cytoplasmatic antibody (ANCA)-associated vasculitis, systemic lupus erythematosus (SLE), monoclonal gammopathy, or amyloidosis [1][2]. In the case of isolated microscopic hematuria without renal function impairment, a biopsy is only indicated in exceptional cases (e.g., for clarification before potential living donation), as there is usually no therapeutic consequence due to an overall favorable prognosis [1]. However, the kidney biopsy renders it possible to distinguish the underlying entities. The most frequent differential diagnoses include immunoglobin A (IgA) nephropathy, hereditary nephritis (classic Alport syndrome), and thin basement membrane syndrome, which, according to recent findings, is attributed to the autosomal recessive form of Alport syndrome in the case of heterozygosity [19][20][21]. In instances of mild proteinuria below 1 g/24 h without an active sediment and without clinical or serological evidence of a systemic disease, many nephrologists relativize the indication for renal biopsy [1][2]. Immunosuppressive therapy is usually not indicated. However, these patients require regular monitoring. If proteinuria increases, hypertension occurs and/or renal function decreases, a histological clarification should be sought [2]. Biopsy of nephrotic syndrome in childhood is usually not necessary. In more than 90% of cases, glomerular minimal lesions are present that respond very well to steroids. However, in steroid-resistant nephrotic syndrome, renal biopsy is indicated and can be performed safely [22][23].
In adults, membranous nephropathy (MN) and focal segmental glomerulosclerosis are among the most common causes of nephrotic syndrome, ahead of minimal glomerular lesions. Unexpected diagnoses, such as primary amyloidosis, fibrillary or immunotactoid glomerulopathy, and rare diseases, such as Fabry disease, expand the differential diagnostic spectrum with the resulting therapeutic implications. In recent years, antibodies to target antigens on podocytes underlying primary MN have been identified, namely antibodies to phospholipase A2 receptor (PLA2R-Abs) and, less frequently, to thrombospondin type-1 domain-containing protein 7A (THSD7A-Abs) [24][25]. Although it is clear that a kidney biopsy is required in the absence of PLA2R-Abs, their detection in serum is so specific that histological clarification in new-onset nephrotic syndrome is not necessary. Studies have reliably shown that a biopsy at an eGFR of >60 mL/min does not provide an additional diagnosis that would change clinical management, nor does it provide additional information about chronicity or prognosis [26].
Acute nephritic syndrome, clinically characterized by hematuria with microscopic evidence of acanthocytes and/or red blood cell casts, new-onset arterial hypertension, and renal insufficiency, definitely requires biopsy clarification to establish the diagnosis and further therapy [1][2]. It occurs isolated to the kidneys but also in association with immunological systemic disease (e.g., SLE, ANCA-associated vasculitis, and rarely anti-glomerular basal membrane (anti-GBM) nephritis). In ANCA-associated vasculitis, renal histology provides important information on whether the disease is active. Particularly in myeloperoxidase (MPO)-positive disease when confined to the kidneys without other systemic disease symptoms, a biopsy is essential for the indication of immunosuppressive therapy and also for renal prognosis, as it cannot be reliably estimated from conventional laboratory data of sediment, serum creatinine, and autoimmune serology. It has been shown that the number of unaffected normal glomeruli in a representative biopsy not only predicts response to therapy but also provides a prognosis for recovery of renal function after one year [27].
In lupus nephritis, immunosuppressive therapy depends largely on the pattern of involvement and the extent of active or chronic (scarred) lesions [28][29], which cannot be differentiated clinically. Repeated kidney biopsies may also be indicated, as the histological classification criteria overlap considerably and, due to the relapsing course of the disease under immunosuppressive therapy, non-proliferative forms of nephritis often change into proliferative forms and vice versa. Thus, individual patients can pass through different lupus nephritis classes in the course of their disease, with corresponding therapeutic implications [30].
Acute renal failure (prerenal renal failure and acute tubular necrosis) usually does not require a biopsy as long as a typical history and clinical circumstances make the diagnosis plausible [2]. On the other hand, a biopsy should be sought in the case of otherwise unexplained, newly occurring renal function impairment, especially for the etiological clarification of drug toxic causes [2]. In instances of suspected drug-induced acute interstitial nephritis (AIN), the identification of the culprit substance is not always easy because of the broad spectrum of possible substances. The injurious immunologic reaction in AIN is a cell-mediated process that usually manifests 7 to 10 days after exposure to the culprit substance [31]. Thus, clinical workup of AIN requires an accurate history of concomitant medication, including self-medications, the determination of the period between exposure and onset as accurately as possible, and the exclusion of other autoimmune or infectious diseases [32]. Frequent causative substances are analgesics of the non-steroidal anti-inflammatory drug (NSAID) type, which are usually available over the counter, but also several antibiotics and proton pump inhibitors (PPIs) [33]. It is necessary to identify the causative substance as precisely as possible because affected patients have to avoid it for the rest of their lives.
In more recent times, several indications for doing a renal biopsy have evolved from the use of novel tumor therapies in modern oncology. These therapies include tyrosine kinase inhibitors, which quite often confer direct nephrotoxic effects [34][35], but also monoclonal antibodies or recombinant fusion proteins directed against vascular endothelial growth factor (VEGF) or its receptor (bevacizumab and aflibercept), and checkpoint inhibitors [36][37]. Checkpoint inhibitors targeting immune proteins on T cells, such as programmed cell death 1 (PD-1) protein or its ligand (PDL-1), and cytotoxic T lymphocyte antigen 4 (CTLA-4), are frequently associated with various immune phenomena involving the kidneys, such as interstitial nephritis, TMA, and podocytopathy [36][38][39]. When renal function deteriorates or proteinuria occurs, with or without sediment findings, knowledge of renal histology can be helpful not only in characterizing the underlying cause but also in deciding on therapeutic measures to be taken to restore kidney function [39][40]. Sometimes, even effective tumor therapy must be interrupted or discontinued, and it may be necessary to switch to an alternative regimen and also consider systemic therapy with corticosteroids or immunosuppressants. It is not uncommon for a therapeutic dilemma to arise that requires close collaboration between oncologists and nephrologists.
Renal graft biopsy is the method of choice for the diagnosis and resulting treatments of various allograft injuries, including acute or chronic active rejection [41], BK polyomavirus-associated nephropathy [42], calcineurin inhibitor toxicity, and recurrent or de novo glomerular disease [43]. Due to the variety of mostly therapeutically modifiable disorders of graft function [44], biopsies of transplant kidneys (and re-biopsies) are performed more frequently than those of native kidneys. An indication in the early postoperative phase is generally given in cases of primary non-function, suspected acute rejection, or nonresponse to rejection therapy, but usually also in cases of deterioration of graft function in the further course or if proteinuria is detected above 1–2 g/24 h. Kidney allograft rejection has been graded according to the Banff Classification since 1991 [45], which has been revised and further developed over the years by an international expert panel of nephrologists, transplant surgeons, and pathologists at regular meetings. Key points of the most recent Banff 2019 classification mainly focused on the refinements to the criteria for chronic active T cell-mediated rejection (TCMR), borderline rejection, and antibody-mediated rejection (ABMR). In addition, the Banff Molecular Working Group (BMWG) elaborated a multiorgan gene panel, which is hoped to enable a pathogenesis and pathway-based molecular approach for diagnostics and therapeutic decision making [9][41].
Table 1. Indication for renal biopsy.
Biopsy of the native kidney to diagnose unknown renal disease
 Adult nephrotic syndrome [1][2]
  Excepting new-onset nephrotic syndrome with evidence of PLA2-R-Abs [24][26]
 Proteinuria > 1–2 g/24 h with or without hypertension [2]
  Excepting proteinuria/albuminuria associated with diabetes mellitus in the presence of proven diabetic
  retinopathy [2]
 Progressive increase in serum creatinine with microscopic evidence of acanthocytes and/or red blood cell casts [1][2]
 Systemic diseases (immunological or paraneoplastic) with suspected renal involvement [1][2]
  e.g., clinical/serologic evidence of systemic vasculitis c/p-ANCA positive and PR3-/MPO-Abs positive [1][2][27]
  e.g., clinical/serologic evidence of systemic lupus erythematosus (SLE) [1][2][30]
  e.g., serologic evidence of monoclonal gammopathy [1]
 Impaired renal function of unclear etiology (if kidneys are of normal size on ultrasound) with or without sterile
 pyuria/white blood cell casts/low-grade proteinuria [1][2]
  e.g., drug-induced interstitial nephritis [2][31][33]
  e.g., interstitial nephritis related to autoimmune diseases (sarcoidosis, IgG4-related disease) [2]
Repeated biopsy to examine severity of damage or progression of an already-known kidney disease
 Nonresponse to an established therapy [22][23]
  e.g., steroid resistance with glomerular minimal lesions
 Therapy monitoring [1][2][30]
  e.g., clarification of whether immunosuppressive therapy needs to be intensified or can be suspended in
  individual cases of SLE or ANCA-associated vasculitis
 Recurrent disease activity [1][2][27][30]
  e.g., evaluation of active/chronic (scarring) lesions prior to resumption of immunosuppressive therapy.
Biopsy of the renal graft
 All the conditions of the native kidney
Special considerations for the kidney transplant
 Primary non-function after transplantation
  Differentiation of acute tubular necrosis (ATN) from early rejection [41]
 Rapid graft function impairment, in particular when rejection is suspected
  Grading according to Banff classification with regard to prognosis and treatment [41]
  Kind of rejection (cellular/antibody-mediated) [41]
  Differentiation of active/chronic lesions [41]
 Clarification of nonresponse to rejection therapy
  Guidance of intensified immunosuppressive therapy [44]
  Detection/exclusion of infectious causes (BK-polyoma nephropathy) [42]
 Deterioration of graft function in the ongoing course with or without proteinuria > 1–2 g/24 h
  Differentiation of chronic active rejection/late onset rejection/tubulointerstitial fibrosis (IFTA) [41]
  Diagnosis of recurrent kidney disease [43]
  Recognition of drug toxicities (calcineurin inhibitor toxicity) [41]
 Control biopsies at predetermined time points (in context of clinical trials only)
Abbreviations: PLA2-R-Abs: phospholipase A2-receptor antibodies, c-ANCAs: antineutrophil cytoplasmatic antibodies, p-ANCAs: perinuclear antineutrophil cytoplasmatic antibodies, PR3-Abs: proteinase 3 antibodies, MPO-Abs: myeloperoxidase antibodies, SLE: systemic lupus erythematosus, and IgG4: immunoglobulin G4.

References

  1. Hogan, J.J.; Mocanu, M.; Berns, J.S. The Native Kidney Biopsy: Update and Evidence for Best Practice. Clin. J. Am. Soc. Nephrol. 2016, 11, 354–362.
  2. Luciano, R.L.; Moeckel, G.W. Update on the Native Kidney Biopsy: Core Curriculum 2019. Am. J. Kidney Dis. 2019, 73, 404–415.
  3. Corapi, K.M.; Chen, J.L.; Balk, E.M.; Gordon, C.E. Bleeding complications of native kidney biopsy: A systematic review and meta-analysis. Am. J. Kidney Dis. 2012, 60, 62–73.
  4. Poggio, E.D.; McClelland, R.L.; Blank, K.N.; Hansen, S.; Bansal, S.; Bomback, A.S.; Canetta, P.A.; Khairallah, P.; Kiryluk, K.; Lecker, S.H.; et al. Systematic Review and Meta-Analysis of Native Kidney Biopsy Complications. Clin. J. Am. Soc. Nephrol. 2020, 15, 1595–1602.
  5. Fogo, A.B. Approach to renal biopsy. Am. J. Kidney Dis. 2003, 42, 826–836.
  6. Walker, P.D.; Cavallo, T.; Bonsib, S.M.; Ad Hoc Committee on Renal Biopsy Guidelines of the Renal Pathology Society. Practice guidelines for the renal biopsy. Mod. Pathol. 2004, 17, 1555–1563.
  7. Chang, A.; Gibson, I.W.; Cohen, A.H.; Weening, J.J.; Jennette, J.C.; Fogo, A.B. Renal Pathology Society. A position paper on standardizing the nonneoplastic kidney biopsy report. Clin. J. Am. Soc. Nephrol. 2012, 7, 1365–1368.
  8. Williams, W.W.; Taheri, D.; Tolkoff-Rubin, N.; Colvin, R.B. Clinical role of the renal transplant biopsy. Nat. Rev. Nephrol. 2012, 8, 110–121.
  9. Mengel, M.; Loupy, A.; Haas, M.; Roufosse, C.; Naesens, M.; Akalin, E.; Clahsen-van Groningen, M.C.; Dagobert, J.; Demetris, A.J.; Duong van Huyen, J.P.; et al. Banff 2019 Meeting Report: Molecular diagnostics in solid organ transplantation-Consensus for the Banff Human Organ Transplant (B-HOT) gene panel and open source multicenter validation. Am. J. Transplant. 2020, 20, 2305–2317.
  10. Jansen, J.; Reimer, K.C.; Nagai, J.S.; Varghese, F.S.; Overheul, G.J.; de Beer, M.; Roverts, R.; Daviran, D.; Fermin, L.A.S.; Willemsen, B.; et al. SARS-CoV-2 infects the human kidney and drives fibrosis in kidney organoids. Cell Stem Cell 2022, 29, 217–231.
  11. Puelles, V.G.; Lütgehetmann, M.; Lindenmeyer, M.T.; Sperhake, J.P.; Wong, M.N.; Allweiss, L.; Chilla, S.; Heinemann, A.; Wanner, N.; Liu, S.; et al. Multiorgan and Renal Tropism of SARS-CoV-2. N. Engl. J. Med. 2020, 383, 590–592.
  12. Richards, N.T.; Darby, S.; Howie, A.J.; Adu, D.; Michael, J. Knowledge of renal histology alters patient management in over 40% of cases. Nephrol. Dial. Transplant. 1994, 9, 1255–1259.
  13. Pascual, M.; Vallhonrat, H.; Cosimi, A.B.; Tolkoff-Rubin, N.; Colvin, R.B.; Delmonico, F.L.; Ko, D.S.; Schoenfeld, D.A.; Williams, W.W., Jr. The clinical usefulness of the renal allograft biopsy in the cyclosporine era: A prospective study. Transplantation. 1999, 67, 737–741.
  14. Fuiano, G.; Mazza, G.; Comi, N.; Caglioti, A.; De Nicola, L.; Iodice, C.; Andreucci, M.; Andreucci, V.E. Current indications for renal biopsy: A questionnaire-based survey. Am. J. Kidney Dis. 2000, 35, 448–457.
  15. Burke, J.P.; Pham, T.; May, S.; Okano, S.; Ratanjee, S.K.; Thet, Z.; Wong, J.K.W.; Venuthurupalli, S.; Ranganathan, D. Kidney biopsy practice amongst Australasian nephrologists. BMC Nephrol. 2021, 22, 291.
  16. Bollee, G.; Martinez, F.; Moulin, B.; Meulders, Q.; Rougier, J.P.; Baumelou, A.; Glotz, D.; Subra, J.F.; Ulinski, T.; Vrigneaud, L.; et al. Renal biopsy practice in France: Results of a nationwide study. Nephrol. Dial. Transplant. 2010, 25, 3579–3585.
  17. Kawaguchi, T.; Nagasawsa, T.; Tsuruya, K.; Miura, K.; Katsuno, T.; Morikawa, T.; Ishikawa, E.; Ogura, M.; Matsumura, H.; Kurayama, R.; et al. A nationwide survey on clinical practice patterns and bleeding complications of percutaneous native kidney biopsy in Japan. Clin. Exp. Nephrol. 2020, 24, 389–401.
  18. Briganti, E.M.; Dowling, J.; Finlay, M.; Hill, P.A.; Jones, C.L.; Kincaid-Smith, P.S.; Sinclair, R.; McNeil, J.J.; Atkins, R.C. The incidence of biopsy-proven glomerulonephritis in Australia. Nephrol. Dial. Transplant. 2001, 16, 1364–1367.
  19. Torra, R.; Furlano, M.; Ars, E. How genomics reclassifies diseases: The case of Alport syndrome. Clin. Kidney J. 2020, 13, 933–935.
  20. Gibson, J.; Fieldhouse, R.; Chan, M.M.Y.; Sadeghi-Alavijeh, O.; Burnett, L.; Izzi, V.; Persikov, A.V.; Gale, D.P.; Storey, H.; Savige, J. Genomics England Research Consortium. Prevalence Estimates of Predicted Pathogenic COL4A3-COL4A5 Variants in a Population Sequencing Database and Their Implications for Alport Syndrome. J. Am. Soc. Nephrol. 2021, 32, 2273–2290.
  21. Savige, J.; Lipska-Zietkiewicz, B.S.; Watson, E.; Hertz, J.M.; Deltas, C.; Mari, F.; Hilbert, P.; Plevova, P.; Byers, P.; Cerkauskaite, A.; et al. Guidelines for Genetic Testing and Management of Alport Syndrome. Clin. J. Am. Soc. Nephrol. 2022, 17, 143–154.
  22. Nammalwar, B.R.; Vijayakumar, M.; Prahlad, N. Experience of renal biopsy in children with nephrotic syndrome. Pediatr. Nephrol. 2006, 21, 286–288.
  23. Varnell CDJr Stone, H.K.; Welge, J.A. Bleeding Complications after Pediatric Kidney Biopsy: A Systematic Review and Meta-Analysis. Clin J Am Soc Nephrol. 2019, 14, 57–65.
  24. Beck, L.H., Jr.; Bonegio, R.G.B.; Lambeau, G.; Beck, D.M.; Powell, D.W.; Cummins, T.D.; Klein, J.B.; Salant, D. M-type phospholipase A 2 receptor as target antigen in idiopathic membranous nephropathy. N. Engl. J. Med. 2009, 361, 11–21.
  25. Tomas, N.M.; Beck, L.H., Jr.; Meyer-Schwesinger, C.; Seitz-Polski, B.; Ma, H.; Zahner, G.; Dolla, G.; Hoxha, E.; Helmchen, U.; Dabert-Gay, A.S.; et al. Thrombospondin type-1 domain-containing 7A in idiopathic membranous nephropathy. N. Engl. J. Med. 2014, 371, 2277–2287.
  26. McDonnell, T.; Wu, H.H.L.; Sinha, S.; Chinnadurai, R. The Role of PLA2R in Primary Membranous Nephropathy: Do We Still Need a Kidney Biopsy? Genes 2023, 14, 1343.
  27. Bajema, I.M.; Hagen, E.C.; Hermans, J.; Noël, L.H.; Waldherr, R.; Ferrario, F.; Van Der Woude, F.J.; Bruijn, J.A. Kidney biopsy as a predictor for renal outcome in ANCA-associated necrotizing glomerulonephritis. Kidney Int. 1999, 56, 1751–1758.
  28. Weening, J.J.; D’Agati, V.D.; Schwartz, M.M.; Seshan, S.V.; Alpers, C.E.; Appel, G.B.; Balow, J.E.; Bruijn, J.A.; Cook, T.; Ferrario, F.; et al. The classification of glomerulonephritis in systemic lupus erythematosus revisited. J. Am. Soc. Nephrol. 2004, 15, 241–250.
  29. Bajema, I.M.; Wilhelmus, S.; Alpers, C.E.; Bruijn, J.A.; Colvin, R.B.; Cook, H.T.; D’Agati, V.D.; Ferrario, F.; Haas, M.; Jennette, J.C.; et al. Revision of the International Society of Nephrology/Renal Pathology Society classification for lupus nephritis: Clarification of definitions, and modified National Institutes of Health activity and chronicity indices. Kidney Int. 2018, 93, 789–796.
  30. Yu, F.; Haas, M.; Glassock, R.; Zhao, M.H. Redefining lupus nephritis: Clinical implications of pathophysiologic subtypes. Nat. Rev. Nephrol. 2017, 13, 483–495.
  31. Raghavan, R.; Shawar, S. Mechanisms of Drug-Induced Interstitial Nephritis. Adv. Chronic Kidney Dis. 2017, 24, 64–71.
  32. Schnuelle, P.; Schwab, C.; Waldherr, R.; Zeier, M.; Bischofs, C. Biopsy-proven acute interstitial nephritis after SARS-CoV-2 mRNA vaccination-adverse vaccine side effect or unrelated complication from self-medication? Lessons for the clinical nephrologist. J. Nephrol. 2023, 36, 631–633.
  33. Praga, M.; González, E. Acute interstitial nephritis. Kidney Int. 2010, 77, 956–961.
  34. Huang, L.; Jiang, S.; Shi, Y. Tyrosine kinase inhibitors for solid tumors in the past 20 years (2001–2020). J Hematol Oncol. 2020, 13, 143.
  35. Xiong, Y.; Wang, Q.; Liu, Y.; Wei, J.; Chen, X. Renal adverse reactions of tyrosine kinase inhibitors in the treatment of tumours: A Bayesian network meta-analysis. Front. Pharmacol. 2022, 13, 1023660.
  36. Jhaveri, K.D.; Wanchoo, R.; Sakhiya, V.; Ross, D.W.; Fishbane, S. Adverse Renal Effects of Novel Molecular Oncologic Targeted Therapies: A Narrative Review. Kidney Int. Rep. 2016, 2, 108–123.
  37. Shiravand, Y.; Khodadadi, F.; Kashani, S.M.A.; Hosseini-Fard, S.R.; Hosseini, S.; Sadeghirad, H.; Ladwa, R.; O’Byrne, K.; Kulasinghe, A. Immune Checkpoint Inhibitors in Cancer Therapy. Curr. Oncol. 2022, 29, 3044–3060.
  38. Wanchoo, R.; Karam, S.; Uppal, N.N.; Barta, V.S.; Deray, G.; Devoe, C.; Launay-Vacher, V.; Jhaveri, K.D.; Cancer and Kidney International Network Workgroup on Immune Checkpoint Inhibitors. Adverse Renal Effects of Immune Checkpoint Inhibitors: A Narrative Review. Am. J. Nephrol. 2017, 45, 160–169.
  39. Gupta, S.; Short, S.A.P.; Sise, M.E.; Prosek, J.M.; Madhavan, S.M.; Soler, M.J.; Ostermann, M.; Herrmann, S.M.; Abudayyeh, A.; Anand, S.; et al. ICPi-AKI Consortium Investigators. Acute kidney injury in patients treated with immune checkpoint inhibitors. J. Immunother. Cancer 2021, 9, e003467.
  40. Moss, E.M.; Perazella, M.A. The role of kidney biopsy in immune checkpoint inhibitor nephrotoxicity. Front. Med. 2022, 9, 964335.
  41. Loupy, A.; Haas, M.; Roufosse, C.; Naesens, M.; Adam, B.; Afrouzian, M.; Akalin, E.; Alachkar, N.; Bagnasco, S.; Becker, J.U.; et al. The Banff 2019 Kidney Meeting Report (I): Updates on and clarification of criteria for T cell- and antibody-mediated rejection. Am. J. Transplant. 2020, 20, 2318–2331.
  42. Nickeleit, V.; Singh, H.K.; Randhawa, P.; Drachenberg, C.B.; Bhatnagar, R.; Bracamonte, E.; Chang, A.; Chon, W.J.; Dadhania, D.; Davis, V.G.; et al. The Banff Working Group Classification of definitive polyomavirus nephropathy: Morphologic definitions and clinical correlations. J. Am. Soc. Nephrol. 2018, 29, 680–693.
  43. Uffing, A.; Hullekes, F.; Riella, L.V.; Hogan, J.J. Recurrent glomerular disease after kidney transplantation: Diagnostic and management dilemmas. Clin. J. Am. Soc. Nephrol. 2021, 16, 1730–1742.
  44. Alasfar, S.; Kodali, L.; Schinstock, C.A. Current Therapies in Kidney Transplant Rejection. J. Clin. Med. 2023, 12, 4927.
  45. Solez, K.; Axelsen, R.A.; Benediktsson, H.; Burdick, J.F.; Cohen, A.H.; Colvin, R.B.; Croker, B.P.; Droz, D.; Dunnill, M.S.; Halloran, P.F.; et al. International standardization of criteria for the histologic diagnosis of renal allograft rejection: The Banff working classification of kidney transplant pathology. Kidney Int. 1993, 44, 411–422.
More
© Text is available under the terms and conditions of the Creative Commons Attribution (CC BY) license; additional terms may apply. By using this site, you agree to the Terms and Conditions and Privacy Policy.
Upload a video for this entry
Information
Subjects: Urology & Nephrology
Contributor MDPI registered users' name will be linked to their SciProfiles pages. To register with us, please refer to https://encyclopedia.pub/register :
Peter Schnuelle
View Times: 298
Revisions: 2 times (View History)
Update Date: 06 Nov 2023
Table of Contents
    1000/1000
    Hot Most Recent
    Video Production Service
    Feedback