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Renal Disease; Fluid and Electrolyte Disorders
Published in John S. Axford, Chris A. O'Callaghan, Medicine for Finals and Beyond, 2023
In chronic interstitial nephritis there is, by definition, irreversible structural damage and scarring, but treatment of the cause may slow progression. Papillary necrosis (necrosis of the renal papillae) can arise particularly with drugs (notably the analgesic phenacetin, which is no longer available), sickle cell anaemia and infection (especially in diabetes mellitus or in combination with urinary tract obstruction). Imaging may reveal papillary damage.
An Overview of Drug-Induced Nephropathies *
Published in Robin S. Goldstein, Mechanisms of Injury in Renal Disease and Toxicity, 2020
Jean Paul Fillastre, Michel Godin
Phenindione is now much less prescribed than in last years and this probably explains why no recent cases of acute interstitial nephritis due to this drug were described. Typically, patients presented with fever, rash, eosinophilia, oliguria, and often jaundice. The outcome was severe, most patients dying, but these observations are old and hemodialysis was not performed in some patients. Chronic interstitial nephritis could appear.
Diagnostic Approach to Acute Kidney Injury in the Critical Care Unit
Published in Cheston B. Cunha, Burke A. Cunha, Infectious Diseases and Antimicrobial Stewardship in Critical Care Medicine, 2020
Sonali Gupta, Divyansh Bajaj, Sana Idrees, Joseph Mattana
Acute interstitial nephritis can be secondary to many conditions, most commonly resulting from medication use [29]. In about one-third of cases, there is a history of maculopapular erythematous rash, fever, and arthralgia. Sterile pyuria with eosinophiluria and peripheral eosinophilia are classical findings, but as with some of the physical examination findings, they may be absent, and kidney biopsy may be needed to distinguish between acute interstitial nephritis and other causes of AKI. Acute events involving the renal arteries or veins can also lead to intrinsic AKI, such as with embolic events from atrial fibrillation and a mural cardiac thrombus, as well as in situ thrombosis, as can occur with severe hypotension and stasis in a patient with underlying renovascular atherosclerotic disease. A more common cause of vascular disease-causing AKI is renal atheroembolic disease as may occur following arterial catheterization, vascular surgery, or anticoagulation. A detailed review of these disorders is beyond the scope of this chapter.
Combination therapy with immune check point inhibitors and acute kidney injury
Published in Acta Oncologica, 2023
Amalie Valentin, Anne Kirstine Hundahl Møller, Jesper Andreas Palshof, Bo Broberg, Eva Gravesen, Inge Marie Svane, Ditte Hansen
The causes of AKI are shown in Table 1. Two patients had potential ICI-related AKI, CTCAE grade 2 and 3 respectively (graded using baseline p-creatinine). The interval from the initiation of ipilimumab and nivolumab to the occurrence of ICI-related AKI was 50 days and 84 days respectively. Both patients received treatment with high doses of methylprednisolone with significant improvement of kidney function, but some degree of chronic kidney disease remained in both (CKD stage 2 and 4 respectively). One of these patients underwent a kidney biopsy showing acute interstitial nephritis. This patient had a relapse of ICI-related AKI 11 months after receiving treatment with ipilimumab and nivolumab. This also responded with a partial remission to methylprednisolone treatment (Figure 1). None of the patients was treated with second-line immunosuppressive drugs. The other patient with potential ICI-related AKI in this group experienced a relapse with increasing p-creatinine while still treated with low-dose glucocorticoids for an ICI–related AKI. This responded to an increased dose of glucocorticoids and a prolonged treatment period. Blood samples revealed a slightly elevated eosinophil count in the patient.
Beneficial effect of fresh frozen plasma in reducing renal complications in Hemiscorpius lepturus scorpion envenomated children with severe hemoglobinuria: an open label randomized clinical trial
Published in Toxin Reviews, 2023
Ehsan Valavi, Parisa Amoori, Neda Mohtasham, Tahereh Ziaei Kajbaf, Mehri Taheri, Bahman Cheraghian, Soodeh Hooshmandi
Scorpion venom causes an inflammatory reaction in the kidneys. The direct toxic effects of venom, release of cytokines, and dilation of vessels can cause interstitial nephritis and ischemic tubular necrosis (Naqvi 2015). Pyuria was significantly associated with AKI, as reported in almost 65% of AKI patients; this indicates the infiltration of leukocytes into the renal parenchyma, which is involved in the development of acute interstitial nephritis. Acute interstitial nephritis can exacerbate renal dysfunction, as mentioned in other studies (Gmar-Bouraoui et al. 2000, Viswanathan and Prabhu 2011). In the present study, despite the low severity of pyuria in the intervention group, the difference was not significant between the two groups. Therefore, use of FFP seems to be relatively effective in reducing leukocyte infiltration into the renal parenchyma, indicating a decline in renal damage in the FFP group.
Urinary T cells are detected in patients with immune checkpoint inhibitor-associated immune nephritis that are clonotypically identical to kidney T cell infiltrates
Published in OncoImmunology, 2022
Shailbala Singh, Leticia C. Clemente, Edwin R. Parra, Amanda Tchakarov, Chao Yang, Yisheng Li, James P. Long, Cassian Yee, Jamie S. Lin
Immune checkpoint inhibitor (ICI) therapy can be a highly effective cancer treatment option, but its use is often limited by the development of autoimmune side effects targeting normal tissues, termed immune-related adverse events (irAEs). While the frequency of acute kidney injury (AKI) in patients receiving ICI therapy is over 15%, immune nephritis is observed in 2–5% of the patients experiencing ICI-associated irAEs.1,2 The most common pathology associated with immune nephritis is acute interstitial nephritis (AIN), an inflammatory renal lesion characterized by a T-lymphocytic tubulointerstitial infiltrates.2 However, other autoimmune pathologies such as glomerulonephritis (GN) and vasculitis can also develop.3 Unlike patients suffering from AKI mediated by other causes, those with ICI-AKI (i.e. AIN, GN, and vasculitis) directly benefit from immune suppressive therapies.4 Differentiating ICI-associated immune nephritis from other causes of AKI (e.g. dehydration, obstruction, sepsis, etc.) herein referred to as non-ICI AKI can be complicated since conventional blood and urine tests are nonspecific in identifying AKI etiology. The risk of major bleeding associated with kidney biopsy in cancer patients further poses a challenge due to elevated risk of morbidity and mortality.5–8 A means to noninvasively screen for ICI-immune nephritis will enable timely diagnosis, improve patient management, and obviate complication risks from invasive diagnostic procedures (i.e. kidney biopsy).