The Case | A 64-year-old woman with retroperitoneal fibrosis, acute kidney injury, and active urine sediment

2021 ◽  
Vol 99 (2) ◽  
pp. 493-494
Author(s):  
Rute Aguiar ◽  
Allifia Abbas ◽  
Catherine Horsfield ◽  
Dimitrios-Anestis Moutzouris
2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Sahra Pajenda ◽  
Sebastian Kapps ◽  
Daniela Gerges ◽  
Gregor Hoermann ◽  
Ludwig Wagner ◽  
...  

Abstract Background Immunosuppression in solid organ transplantation is associated with frequent infections. Renal allograft recipients are susceptible to opportunistic infections and can acquire human cytomegalovirus (HCMV) infections even within the allograft. There, HCMV can be found in both the glomerulus and tubular cells, but is mostly restricted to specific and circumscribed sites. Therefore, not all organ infections are identifiable by immunohistology for HCMV proteins in fine needle core biopsies. Thus, we performed a urinalysis study to search for HCMV-specific RNA transcripts in the urine sediment of patients with acute kidney injury. Methods Urinary sediment of 90 patients with acute kidney injury (AKI), including 48 renal transplant recipients (RTX) and 42 non-transplant recipients (nRTX), was collected from morning urine for RNA extraction and reverse transcription. The copy number of HCMV transcripts was evaluated using a UL132 HCMV-specific probe set and by real-time quantitative polymerase chain reaction (RT-qPCR). Results Of the 48 RTX patients, ten showed HCMV copies in their urine sediment cells. Within this group, three recipients had negative HCMV serology and received an allograft from an HCMV-seropositive donor. In addition, all three RTX patients on a belatacept-based immunosuppressive regimen had HCMV transcripts in their urine. Of the 42 nRTX patients, only two had detectable HCMV transcripts in urine sediment cells and both were under immunosuppression. Conclusions Ten immunosuppressed renal allograft recipients and two immunosuppressed non-transplant patients with AKI showed HCMV copies in urine sediment. Thus, HCMV positivity in urinary sediment appears to be associated with immunosuppression. This study describes a novel noninvasive method for detection of HCMV in urinary sediment. Whether all HCMV infections can be detected or only those with viral replication warrants further investigation.


2010 ◽  
Vol 26 (2) ◽  
pp. 747-751 ◽  
Author(s):  
G. Sandhu ◽  
A. Ranade ◽  
P. Mankal ◽  
L. C. Herlitz ◽  
J. Jones ◽  
...  

2021 ◽  
Author(s):  
Daniel Z. Hodson ◽  
Lloyd G. Cantley ◽  
Sudhir Perincheri ◽  
Nikhil Singh

2021 ◽  
pp. ASN.2021010059
Author(s):  
Paulo Caceres ◽  
Gina Savickas ◽  
Shannon Murray ◽  
Kausik Umanath ◽  
Junior Uduman ◽  
...  

BackgroundAcute kidney injury (AKI) is a complication of coronavirus disease 2019 (COVID-19) that is associated with high mortality. Despite documented kidney tropism of the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), there are no consistent reports of viral detection in urine or correlation with AKI or COVID-19 severity. Here we hypothesize that quantification of SARS-CoV-2 viral load in urine sediment from COVID-19 patients correlates with occurrence of AKI and mortality. MethodsSARS-CoV-2 viral load in urine sediments (U-viral load) was quantified by qRT-PCR in 52 patients with PCR-confirmed COVID-19 diagnosis, hospitalized between March 15th and June 8th, 2020. Immunolabeling of SARS-CoV-2 proteins Spike and Nucleocapsid was performed in two COVID-19 kidney biopsies and urine sediments. Viral infectivity assays were performed from 32 urine sediments. ResultsTwenty COVID-19 patients (39%) had detectable SARS-CoV-2 U-viral load, of which 17 (85%) developed AKI with an average U-viral load 4-times higher than non-AKI COVID-19 patients. U-viral load was highest (7.7-fold) within two weeks after AKI diagnosis. A higher U-viral load correlated with mortality but not with albuminuria or AKI stage. SARS-CoV-2 proteins partially colocalized with the viral receptor ACE2 in kidney biopsies in tubules and parietal cells, and in urine sediment cells. Infective SARS-CoV-2 was not detected in urine sediments. ConclusionOur results further support SARS-CoV-2 kidney tropism. A higher SARS-CoV-2 viral load in urine sediments from COVID-19 patients correlated with increased incidence of AKI and mortality. Urinary viral detection could inform medical care of COVID-19 patients with kidney injury to improve prognosis.


Author(s):  
Shunsuke Shimazaki ◽  
Itsuro Kazukawa ◽  
Kyoko Mori ◽  
Makiko Kihara ◽  
Masanori Minagawa

Summary Ammonium acid urate (AAU) crystals are rare in industrialized countries. Furthermore, the number of children with diabetic ketoacidosis (DKA) who develop severe acute kidney injury (AKI) after hospitalization is small. We encountered two patients with AKI caused by AAU crystals during the recovery phase of DKA upon admission. They were diagnosed with severe DKA and hyperuricemia. Their urine volume decreased and AKI developed several days after hospitalization; however, acidosis improved in both patients. Urine sediment analysis revealed AAU crystals. They were treated with urine alkalization and diuretics. Excretion of ammonia in the urine and urine pH levels increased after treatment of DKA, which resulted in the formation of AAU crystals. In patients with severe DKA, the urine and urine sediment should be carefully examined as AAU can form in the recovery phase of DKA. Learning points Ammonium acid urate crystals could be formed in the recovery phase of diabetic ketoacidosis. Diabetic ketoacidosis patients may develop acute kidney injury caused by ammonium acid urate crystals. Urine and urine sediment should be carefully checked in patients with severe DKA who present with hyperuricemia and volume depletion.


2020 ◽  
Vol 35 (Supplement_3) ◽  
Author(s):  
Moritz Schanz ◽  
Severin Schricker ◽  
Tina Oberacker ◽  
Nora Göbel ◽  
Dominik M Alscher ◽  
...  

Abstract Background and Aims Microscopic examination of urine sediment is a well-established and inexpensive technique for differential diagnosis of acute kidney injury. Especially renal tubular epithelial cells (RTEC) and granular casts (GC) have been shown to be a strong predictor of acute tubule necrosis (ATN), the assumed most common cause for AKI in cardiac surgery patients. So far, no study evaluated urine sediment before manifest AKI is evident. Therefore, the aim of this prospective trial was to evaluate if early changes of urine sediment parameters are indicative for development of acute kidney injury. Method Sequential urine sediment specimens were analyzed on day 0 (d0), day 1 (d1) and day 4 or 5 (d5) after cardiac surgery in n=37 patients. Urine analysis was conducted immediately after collection of urine specimens. Analysis includes detection of RTEC and GC as well as hyaline casts (HC), squamous epithelium (SE), erythrocyte count (EC) and leucocyte count (LC). Urine score (US) - consisting of RTEC and GC - which is described as indicative for ATN, was calculated as described previously. For detection of AKI, serum creatinine, serum cystatin c and urine output were recorded. Urine sediment changes over time were analyzed using differences between day of surgery (d0) and day 1 (d0-d1 = Δd1) or day 5 (d0-d5 = Δd5), respectively. Results Of the 37 included patients n=10 (27%) developed AKI within 5 days. According to the definition of KDIGO 2012, two patients developed Stage 1 (20%), six patients Stage 2 (60%) and two patients Stage 3 (20%) AKI. Median age was 67 years (IQR: 63.5-73.0). Mean HC, GC, RTEC and US tended to be higher in AKI patients from day one after surgery. Looking at the urine sediment changes over time (Median; IQR), Δd1 of RTEC (AKI: 0.65; 0.00 – 1.15 vs. No AKI: 0.00; -0.03 – 0.03; p=0.010), GC (AKI: 0.25; 0.00 – 0.50; No AKI: 0.00; -0.20 – 0.00; p=0.002) and US (AKI: 0.00; -0.25 – 0.00 vs. No AKI: 0.00; 0.00 – 1.00; p=0.047) were significant higher in AKI group. Also HC (AKI: 1.00; 0.00 – 1.00; No AKI: 0.00; -1.25 – 1.00; p>0.05) tended to be higher in AKI on Δd1, whereas SE, EC and LC did not show any trend between both groups. Δd5 did not show any significant result between AKI and non-AKI. Because all of these patients were catheterised, the results on urinary erythrocyte count were interpreted with appropriate caution. Conclusion This is the first study evaluating sequential urine sediment measurements for early detection of AKI in cardiac surgery. According to these preliminary data, Δd1 of RTEC, GC and US is significant higher in AKI, suggesting that an increase from day of surgery to day 1 may be indicative for the development of AKI right before manifest AKI is evident. Therefore sequential urine sediment measurements could be useful for early detection of AKI after cardiac surgery.


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