A multi-center retrospective cohort study defines the spectrum of kidney pathology in Coronavirus 2019 Disease (COVID-19).

Kidney failure is common in patients with Coronavirus Disease-19 (COVID-19), resulting in increased morbidity and mortality. In an international collaboration, 284 kidney biopsies were evaluated to improve understanding of kidney disease in COVID-19. Diagnoses were compared to five years of 63,575 native biopsies prior to the pandemic and 13,955 allograft biopsies to identify diseases that have increased in patients with COVID-19. Genotyping for APOL1 G1 and G2 alleles was performed in 107 African American and Hispanic patients. Immunohistochemistry for SARS-CoV-2 was utilized to assess direct viral infection in 273 cases along with clinical information at the time of biopsy. The leading indication for native biopsy was acute kidney injury (45.4%), followed by proteinuria with or without concurrent acute kidney injury (42.6%). There were more African American patients (44.6%) than patients of other ethnicities. The most common diagnosis in native biopsies was collapsing glomerulopathy (25.8%), which was associated with high-risk APOL1 genotypes in 91.7% of cases. Compared to the five-year biopsy database, the frequency of myoglobin cast nephropathy and proliferative glomerulonephritis with monoclonal IgG deposits was also increased in patients with COVID-19 (3.3% and 1.7%, respectively), while there was a reduced frequency of chronic conditions (including diabetes mellitus, IgA nephropathy, and arterionephrosclerosis) as the primary diagnosis. In transplants, the leading indication was acute kidney injury (86.4%), for which rejection was the predominant diagnosis (61.4%). Direct SARS-CoV-2 viral infection was not identified. Thus, our multi-center large case series identified kidney diseases that disproportionately affect patients with COVID-19 and demonstrated a high frequency of APOL1 high-risk genotypes within this group, with no evidence of direct viral infection within the kidney.

Sodium polystyrene sulfonate for the treatment of acute hyperkalemia: a retrospective study.

BACKGROUND: Hyperkalemia is a common problem in hospitalized patients, especially those with underlying chronic kidney disease, but evidence-based guidelines for its treatment are lacking. Sodium polystyrene sulfonate (SPS), a cation exchange resin first approved by the FDA for the treatment of hyperkalemia in 1958, is frequently used alone or in conjunction with other medical therapies to lower serum potassium. Recently, the safety and efficacy of SPS have come into question based on multiple reported cases of bowel necrosis associated with SPS administration. OBJECTIVE: The primary objective of this study was to evaluate the use of SPS for the treatment of hyperkalemia, at a large tertiary community teaching hospital, to determine its effectiveness and the incidence of related adverse side effects. METHODS: A retrospective chart review was performed on all adult inpatients receiving single-dose SPS at a 466-bed tertiary community teaching hospital over a 3-year period. RESULTS: 501 patients received SPS for the treatment of hyperkalemia during their index hospital stay. Serum potassium levels decreased by 0.93 mEq/L on average at first recheck after SPS administration, with or without additional medical treatments. Our study identified 10 cases of hypernatremia (greater than 145 mEq/L), 31 cases of hypokalemia (less than 3.5 mEq/L), and 2 cases of bowel necrosis related to the administration of SPS. CONCLUSION: Our results suggest a serum potassium reduction of less than 1 mEq/L after administration of SPS for the treatment of acute hyperkalemia. Additionally, this study offers some evidence that the use of SPS may be associated with harm. We further note the need for standardized guidelines for the treatment of hyperkalemia at our institution.

Repeat imaging for intracranial aneurysms in patients with autosomal dominant polycystic kidney disease with initially negative studies: a prospective ten-year follow-up.

Patients with autosomal dominant polycystic kidney disease (ADPKD) have a higher incidence of intracranial aneurysms (ICA) than the general population. These ICA also rupture at an earlier age in patients with ADPKD and are associated with high morbidity and mortality. In a recent study, 25% of patients with ADPKD with a documented ICA demonstrated a new ICA on follow-up. It is not known, however, whether patients with ADPKD who have had a negative ICA imaging study would demonstrate an ICA on a repeat imaging study. Only 2 (2.6%) of 76 patients with ADPKD with an initially negative study demonstrated an ICA on follow-up, despite the high frequency of risk factors such as hypertension, smoking, and a family history of ruptured ICA. The mean length of follow-up was 9.8 yr (median, 9.7 yr). These findings have important health care and economic implications in following patients with ADPKD.

Recurrence of intracranial aneurysms in autosomal-dominant polycystic kidney disease.

BACKGROUND: The natural history of intracranial aneurysms (ICAs) in individuals with autosomal-dominant polycystic kidney disease (ADPKD) is poorly defined. METHODS: We followed twenty ADPKD subjects, eleven with ruptured and nine with intact ICA, for 15.2 +/- 8.1 years (range, 6.0 to 33.2 years). Initial diagnosis was by four-vessel cerebral angiography in eighteen subjects. Follow-up examinations were four-vessel cerebral angiography in fourteen and magnetic resonance angiography (MRA) in six subjects. We examined the occurrence of new ICAs, an increase in size of existing ICAs, recurrent rupture or surgical intervention, and death. RESULTS: Age at initial diagnosis of ICA was 37.7 +/- 10.4 years (range, 20.2 to 53.1 years). Seventeen subjects (85%) had an anterior and three (15%) had a posterior ICA at initial diagnosis. On restudy, five subjects (25%) had a significant change, consisting of new ICAs in a different location in all five and an increase in size of an existing ICA in two of the five. All subjects with ruptured ICA and one subject with intact ICA had undergone surgery at the time of initial diagnosis. Ten subjects (50%) underwent further surgery 8.1 +/- 6.1 years later (1.3 to 17 years). No subject died during follow-up and one subject experienced a recurrent RICA (RICA). We were unable to identify risk factors associated with development of a new ICA or increase in size of an existing ICA. CONCLUSION: Individuals with ADPKD and ICA appear to be at moderate risk for new ICAs and increase in size of existing ICAs; mortality and risk of recurrent rupture, however, appear to be low.

Relationship between renal volume growth and renal function in autosomal dominant polycystic kidney disease: a longitudinal study.

In autosomal dominant polycystic kidney disease (ADPKD), renal function remains normal for many years into adult life while cysts form and expand progressively, starting in childhood. The longitudinal relationships between renal volume growth, hypertension, and renal function loss have not been examined in detail. At the University of Colorado (Denver, CO), 229 adult subjects with ADPKD participated in a longitudinal study from 1985 to 2001. Sequential ultrasound examinations were performed at a mean interval of 7.8 +/- 3.1 years (range, 2.6 to 15.1 years). Renal volume was calculated using a standard formula for a modified ellipsoid. The Modified Diet in Renal Disease equation was used to calculate glomerular filtration rate (GFR). The mean annual increase in renal volume was 46 +/- 55 cm3, and mean annual decline in GFR was 2.4 +/- 2.8 mL/min/1.73 m2. Men had faster renal growth, more severe hypertension, and a faster decline in GFR than women of similar ages. Multiple linear regression showed a significant relationship between rate of change in GFR and renal volume growth rate, initial renal volume, proteinuria, and age at entry. Correlational analysis showed a significant correlation between GFR and renal volume over time (R = -0.53) and between follow-up renal volume and follow-up GFR (R = -0.50) for both men and women. We conclude that renal volume and rate of renal volume growth may be useful markers for disease progression in early stages of ADPKD when GFR is preserved.