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Leicester Publications
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UK Kidney Association Clinical Practice Guideline: Sodium-Glucose Co-transporter-2 (SGLT-2) Inhibition in Adults with Kidney Disease 2023 UPDATE. Roddick AJ, Wonnacott A, Webb D, Watt A, Watson MA, Staplin N, Riding A, Lioudaki E, Kuverji A, Kossi ME, Holmes P, Holloway M, Fraser D, Carvalho C, Burton JO, Bhandari S, Herrington WG, Frankel AH.
Multidisciplinary perspectives on cardiac assessment before kidney transplantation: Results from a UK survey.
Nimmo A, Graham-Brown M, Sharif A, Taylor D, Ravanan R
Using the kidney failure risk equation to predict end-stage kidney disease in CKD patients of South Asian ethnicity: an external validation study.
Maher F, Teece L, Major RW, Bradbury N, Medcalf JF, Brunskill NJ, Booth S, Gray LJ
Estimated Glomerular Filtration Rate, Albuminuria, and Adverse Outcomes: An Individual-Participant Data Meta-Analysis.
Writing Group for the CKD Prognosis Consortium; Grams ME, Coresh J, Matsushita K, Ballew SH, Sang Y, Surapaneni A, Alencar de Pinho N, Anderson A, Appel LJ, Ärnlöv J, Azizi F, Bansal N, Bell S, Bilo HJG, Brunskill NJ, Carrero JJ, Chadban S, Chalmers J, Chen J, Ciemins E, Cirillo M, Ebert N, Evans M, Ferreiro A, Fu EL, Fukagawa M, Green JA, Gutierrez OM, Herrington WG, Hwang SJ, Inker LA, Iseki K, Jafar T, Jassal SK, Jha V, Kadota A, Katz R, Köttgen A, Konta T, Kronenberg F, Lee BJ, Lees J, Levin A, Looker HC, Major R, Melzer Cohen C, Mieno M, Miyazaki M, Moranne O, Muraki I, Naimark D, Nitsch D, Oh W, Pena M, Purnell TS, Sabanayagam C, Satoh M, Sawhney S, Schaeffner E, Schöttker B, Shen JI, Shlipak MG, Sinha S, Stengel B, Sumida K, Tonelli M, Valdivielso JM, van Zuilen AD, Visseren FLJ, Wang AY, Wen CP, Wheeler DC, Yatsuya H, Yamagata K, Yang JW, Young A, Zhang H, Zhang L, Levey AS, Gansevoort RT.
Racial, ethnic and regional differences in the effect of sodium-glucose co-transporter 2 inhibitors and glucagon-like peptide 1 receptor agonists on cardiovascular and renal outcomes: a systematic review and meta-analysis of cardiovascular outcome trials.
Kunutsor SK, Khunti K, Seidu S.
Efficacy and safety of a targeted-release formulation of budesonide in patients with primary IgA nephropathy (NefIgArd): 2-year results from a randomised phase 3 trial.
Lafayette R, Kristensen J, Stone A, Floege J, Tesař V, Trimarchi H, Zhang H, Eren N, Paliege A, Reich HN, Rovin BH, Barratt J; NefIgArd trial investigators.
Kidney transplantation in low- and middle-income countries: the Transplant Links experience.
Roberts LE, Kaur A, Jewitt-Harris J, Ready A, Milford DV.
Kidney Function and Long-Term Risk of End-Stage Kidney Disease and Mortality in a Multiethnic Population.
Ling S, Xu G, Zaccardi F, Khunti K, Brunskill NJ
The NightLife study - the clinical and cost-effectiveness of thrice-weekly, extended, in-centre nocturnal haemodialysis versus daytime haemodialysis using a mixed methods approach: study protocol for a randomised controlled trial.
Hull KL, Bramham K, Brookes CL, Cluley V, Conefrey C, Cooper NJ, Eborall H, Fotheringham J, Graham-Brown MPM, Gray LJ, Mark PB, Mitra S, Murphy GJ, Quann N, Rooshenas L, Warren M, Burton JO
Epidemiology of childhood acute kidney injury in England using e-alerts.
Plumb L, Casula A, Sinha MD, Inward CD, Marks SD, Medcalf J, Nitsch D
IgA nephropathy: the lectin pathway and implications for targeted therapy.
Barratt J, Lafayette RA, Zhang H, Tesar V, Rovin BH, Tumlin JA, Reich HN, Floege J
Effects of atrasentan on markers of liver function in patients with type 2 diabetes and chronic kidney disease.
Kohan DE, Liew A, Tang SCW, Barratt J, Heerspink HJL
Sauna bathing, renal function and chronic kidney disease: Cross-sectional and longitudinal findings from the KIHD study.
Kunutsor SK, Kauhanen J, Laukkanen JA
Multimorbidity prevalence and patterns in chronic kidney disease: findings from an observational multicentre UK cohort study.
Hawthorne G, Lightfoot CJ, Smith AC, Khunti K, Wilkinson TJ.
The role of complement in glomerulonephritis-are novel therapies ready for prime time?
Cheung CK, Dormer JP, Barratt J.
Rationale and design of CONTINUITY: a Phase 4 randomized controlled trial of continued post-discharge sodium zirconium cyclosilicate treatment versus standard of care for hyperkalemia in chronic kidney disease.
Burton JO, Allum AM, Amin A, Linde C, Lesén E, Mellström C, Eudicone JM, Sood MM
Genome-wide association analyses define pathogenic signaling pathways and prioritize drug targets for IgA nephropathy.
Kiryluk K, Sanchez-Rodriguez E, Zhou XJ, Zanoni F, Liu L, Mladkova N, Khan A, Marasa M, Zhang JY, Balderes O, Sanna-Cherchi S, Bomback AS, Canetta PA, Appel GB, Radhakrishnan J, Trimarchi H, Sprangers B, Cattran DC, Reich H, Pei Y, Ravani P, Galesic K, Maixnerova D, Tesar V, Stengel B, Metzger M, Canaud G, Maillard N, Berthoux F, Berthelot L, Pillebout E, Monteiro R, Nelson R, Wyatt RJ, Smoyer W, Mahan J, Samhar AA, Hidalgo G, Quiroga A, Weng P, Sreedharan R, Selewski D, Davis K, Kallash M, Vasylyeva TL, Rheault M, Chishti A, Ranch D, Wenderfer SE, Samsonov D, Claes DJ, Akchurin O, Goumenos D, Stangou M, Nagy J, Kovacs T, Fiaccadori E, Amoroso A, Barlassina C, Cusi D, Del Vecchio L, Battaglia GG, Bodria M, Boer E, Bono L, Boscutti G, Caridi G, Lugani F, Ghiggeri G, Coppo R, Peruzzi L, Esposito V, Esposito C, Feriozzi S, Polci R, Frasca G, Galliani M, Garozzo M, Mitrotti A, Gesualdo L, Granata S, Zaza G, Londrino F, Magistroni R, Pisani I, Magnano A, Marcantoni C, Messa P, Mignani R, Pani A, Ponticelli C, Roccatello D, Salvadori M, Salvi E, Santoro D, Gembillo G, Savoldi S, Spotti D, Zamboli P, Izzi C, Alberici F, Delbarba E, Florczak M, Krata N, Mucha K, Pączek L, et al
Physical activity and nutrition in chronic kidney disease.
Wang AY, March DS, Burton JO.
Budesonide delayed-release capsules to reduce proteinuria in adults with primary immunoglobulin A nephropathy.
Barratt J, Lafayette RA, Rovin BH, Fellström B.
Long-Term Outcomes in IgA Nephropathy.
Pitcher D, Braddon F, Hendry B, Mercer A, Osmaston K, Saleem MA, Steenkamp R, Wong K, Turner AN, Wang K, Gale DP, Barratt J.
Defining myocardial infarction in trials of people receiving hemodialysis: consensus report from the SONG-HD MI Expert Working group.
O'Lone E, Apple FS, Burton JO, Caskey FJ, Craig JC, deFilippi CR, Forfang D, Hicks KA, Jha V, Mahaffey KW, Mark PB, Rossignol P, Scholes-Robertson N, Jaure A, Viecelli AK, Wang AY, Wheeler DC, White D, Winkelmayer WC, Herzog CA.
Associations of health literacy with self-management behaviours and health outcomes in chronic kidney disease: a systematic review.
Billany RE, Thopte A, Adenwalla SF, March DS, Burton JO, Graham-Brown MPM.
Let's get physical: considering and overcoming the barriers to physical activity in CKD.
Stevens KI, Graham-Brown M, Lees JS.
Seasonal mortality trends for hospitalised patients with acute kidney injury across England.
Wong E, Peracha J, Pitcher D, Casula A, Steenkamp R, Medcalf JF, Nitsch D.
Atherosclerotic Renovascular Disease: a clinical practice document by the European Renal Best Practice (ERBP) board of the European Renal Association (ERA) and the Working Group Hypertension and the Kidney of the European Society of Hypertension (ESH).
Sarafidis PA, Theodorakopoulou M, Ortiz A, Fernandez-Fernández B, Nistor I, Schmieder R, Arici M, Saratzis A, Van der Niepen P, Halimi JM, Kreutz R, Januszewicz A, Persu A, Cozzolino M.
Acute Kidney Injury Following Revascularization in Patients With Chronic Limb-Threatening Ischemia and Non-Dialysis-Dependent Chronic Kidney Disease: Insights From the NSQIP Database at 30-Day Follow-Up.
Stavroulakis K, Tsilimparis N, Saratzis A, Rantner B, Stana J, Dayama A, Davies MG, Gouveia E Melo R.
Sparsentan in patients with IgA nephropathy: a prespecified interim analysis from a randomised, double-blind, active-controlled clinical trial.
Heerspink HJL, Radhakrishnan J, Alpers CE, Barratt J, Bieler S, Diva U, Inrig J, Komers R, Mercer A, Noronha IL, Rheault MN, Rote W, Rovin B, Trachtman H, Trimarchi H, Wong MG, Perkovic V; PROTECT Investigators
What data collection methods work best for COVID19 outbreak surveillance for people with end stage kidney disease? An observational cohort study using the UK Renal Registry.
Santhakumaran S, Savino M, Benoy-Deeney F, Steenkamp R, Medcalf J, Nitsch D.
HBSP improves kidney ischemia-reperfusion injury and promotes repair in properdin deficient mice via enhancing phagocytosis of tubular epithelial cells.
Wu Y, Huang L, Sai W, Chen F, Liu Y, Han C, Barker JM, Zwaini ZD, Lowe MP, Brunskill NJ, Yang B.
Digital health interventions in chronic kidney disease: levelling the playing field?
Graham-Brown MPM, Smith AC, Greenwood SA
An update on corticosteroid treatment for IgA nephropathy.
Ghaddar M, Barratt J, Barbour SJ.
First do no harm: systemic glucocorticoids should not be used for the treatment of progressive IgA nephropathy.
Cheung CK, Barratt J.
Safety of Roxadustat Versus Erythropoiesis-Stimulating Agents in Patients with Anemia of Non-dialysis-Dependent or Incident-to-Dialysis Chronic Kidney Disease: Pooled Analysis of Four Phase 3 Studies.
Barratt J, Dellanna F, Portoles J, Choukroun G, De Nicola L, Young J, Dimković N, Reusch M.
Major cardiovascular events and subsequent risk of kidney failure with replacement therapy: a CKD Prognosis Consortium study.
Mark PB, Carrero JJ, Matsushita K, Sang Y, Ballew SH, Grams ME, Coresh J, Surapaneni A, Brunskill NJ, Chalmers J, Chan L, Chang AR, Chinnadurai R, Chodick G, Cirillo M, de Zeeuw D, Evans M, Garg AX, Gutierrez OM, Heerspink HJL, Heine GH, Herrington WG, Ishigami J, Kronenberg F, Lee JY, Levin A, Major RW, Marks A, Nadkarni GN, Naimark DMJ, Nowak C, Rahman M, Sabanayagam C, Sarnak M, Sawhney S, Schneider MP, Shalev V, Shin JI, Siddiqui MK, Stempniewicz N, Sumida K, Valdivielso JM, van den Brand J, Yee-Moon Wang A, Wheeler DC, Zhang L, Visseren FLJ, Stengel B.
Exercise and chronic kidney disease: potential mechanisms underlying the physiological benefits.
Bishop NC, Burton JO, Graham-Brown MPM, Stensel DJ, Viana JL, Watson EL.
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Chronic kidney disease (newly identified): Clinical presentation and diagnostic approach in adults
CLINICAL PRESENTATION
CKD patients may present with symptoms and signs resulting directly from diminished kidney function, such as edema or hypertension. However, many have no clinical symptoms, and kidney disease is often detected in these patients when an elevated serum creatinine, reduced estimated glomerular filtration rate (eGFR), or an abnormal urinalysis is discovered incidentally (when such tests are obtained as part of routine evaluation or for a possibly unrelated disorder). In addition, radiographic findings (eg, small and echogenic kidneys [by ultrasound] suggesting chronic damage, multiple bilateral renal cysts with enlarged kidneys suggestive of polycystic kidney disease) may be observed on imaging performed for some other reason.
Depending upon the duration and severity of CKD, patients may also present with symptoms and/or signs of prolonged kidney failure, including weakness and easy fatigability, anorexia, vomiting, pruritus, and, in very advanced stages, with encephalopathy or seizures.
An abnormally reduced urine output (ie, oliguria or anuria) is seldom observed with CKD alone and always indicates at least some component of acute kidney injury (AKI). Oliguria or anuria may be present among patients with AKI superimposed on CKD, such as may be observed in a patient with chronic obstruction who develops acute urinary retention. Similarly, anuria as a result of severe or prolonged shock, bilateral urinary tract obstruction, pregnancy-related cortical necrosis, or bilateral renal arterial occlusion (eg, due to a dissecting aortic aneurysm) may occur in patients with underlying CKD. (See "Evaluation of acute kidney injury among hospitalized adult patients", section on 'Clinical manifestations'.)
The most common laboratory findings in patients with CKD include increased serum creatinine and blood urea nitrogen. Urine studies may show proteinuria (or albuminuria) and/or abnormal red or white blood cells on urine microscopy. (See "Assessment of kidney function" and "Urinalysis in the diagnosis of kidney disease".)
Other common laboratory abnormalities that may be part of the clinical picture include anemia, hyperphosphatemia, hyperkalemia, metabolic acidosis, hypocalcemia, and elevated parathyroid hormone (PTH).
The degree to which these abnormalities are present depends upon the severity of CKD. Hyperphosphatemia is uncommon among CKD patients with eGFR >45 mL/min/1.73 m2. PTH, on the other hand, may be mildly elevated even with a mild reduction of eGFR (ie, 50 to 60 mL/min/1.73 m2). (See "Overview of chronic kidney disease-mineral and bone disorder (CKD-MBD)", section on 'Overview'.)
COVID-19: Issues related to acute kidney injury, glomerular disease, and hypertension
At the end of 2019, a novel coronavirus (ie, SARS-CoV-2) was identified as the cause of a cluster of pneumonia cases in Wuhan, a city in the Hubei Province of China. By 2020, it led to a pandemic that has spread throughout most countries of the world. SARS-CoV-2 disease (COVID-19) primarily manifests as a lung infection with symptoms ranging from those of a mild upper respiratory infection to severe pneumonia, acute respiratory distress syndrome, and death. COVID-19 disproportionately affects patients with preexisting comorbidities, such as patients with various types of kidney disease.
With the widespread use of vaccinations, availability of antiviral therapy, and the emergence of less pathogenic variants of SARS-CoV-2, many strategies developed to mitigate the effect of COVID-19 on patients with kidney disease are no longer needed. However, it is possible that virulent cases of COVID-19 may surge again in the future. In addition, the response to the COVID-19 pandemic will inform the management of future outbreaks of severe respiratory disease in patients with kidney disease.
This topic will discuss issues related to COVID-19 and delivery of nephrology care in patients with acute kidney injury, glomerular disease, chronic kidney disease, and hypertension. Issues related to the care of patients who have end-stage kidney disease or who are candidates for or have a kidney transplant are discussed separately. (See "COVID-19: Issues related to end-stage kidney disease" and "COVID-19: Issues related to solid organ transplantation".)
Antihypertensive therapy and progression of chronic kidney disease: Experimental studies
Extensive studies in animals and humans have shown that progression of a variety of chronic kidney diseases may be largely due to secondary hemodynamic and metabolic factors, rather than the activity of the underlying disorder. Identification of these factors, such as intraglomerular hypertension and glomerular hypertrophy, is important clinically because they can be treated, possibly preventing or minimizing further glomerular injury [1-3]. A review of the mechanisms by which these alterations might occur and how they might induce glomerular injury is available elsewhere. (See "Secondary factors and progression of chronic kidney disease".)
An important component of this approach is antihypertensive therapy with blockers of the renin angiotensin system (RAS), specifically use of angiotensin-converting enzyme (ACE) inhibitors or angiotensin receptor blockers (ARBs). The experimental studies supporting this approach will be reviewed here. The clinical trials and recommendations are presented separately. (See "Antihypertensive therapy and progression of nondiabetic chronic kidney disease in adults".)
PREFERENTIAL EFFECT OF RAS BLOCKERS ON RENAL HEMODYNAMICS
From a therapeutic viewpoint, lowering systemic blood pressure is beneficial in a variety of experimental kidney diseases, at least in part by reducing intraglomerular pressure [1,2,4-6]. Renin angiotensin system (RAS) blockers, including angiotensin-converting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARBs), appear to be particularly effective in this regard; this effect may be related to reversal of the angiotensin II-induced increase in resistance at the efferent or postglomerular arteriole [4,5]. Dilation of the efferent arteriole will facilitate blood movement out of the glomerulus, lowering the intraglomerular pressure independent of any change in systemic blood pressure. A brief review of the actions of angiotensin II on glomerular hemodynamics is available elsewhere. (See "Renal effects of ACE inhibitors in hypertension".)
It is presumed that the deleterious effect of angiotensin II represents local generation since circulating levels are normal or reduced (due to volume expansion) in many patients with chronic kidney disease [7]. In the remnant kidney model of chronic kidney failure, for example, endothelial injury or activation is associated with enhanced expression of angiotensinogen mRNA, which may then lead to increases in angiotensinogen and angiotensin II production [8].
Angiotensin receptor blockers — Data in animal models have found that ARBs are as effective as ACE inhibitors [9-13], albeit with a lesser antiproteinuric effect [14,15].
With experimental models, some variability in results may be due to differences in dosing, which was mostly based on the maximal blood pressure reductions. In some experimental studies, much higher levels of the angiotensin-I receptor are noted in kidney parenchyma than in vascular smooth muscle cells [16]. This suggests that higher doses of ARBs may be required to effectively block kidney parenchymal receptors than the doses used to lower blood pressure. These much higher doses may confer effects beyond that obtained with blood pressure lowering, particularly decreased inflammation and superior nephroprotection.
This hypothesis was evaluated in the 5/6 renal ablation model in which conventional doses of losartan (L50), supplemented with hydrochlorothiazide and hydralazine to achieve similar blood pressures, were compared with 10-fold higher doses of losartan (L500) [17]. Among the effects measured, glomerular pressure and glomerular filtration rate were similar with both L50 and L500, although blood pressure and renal vascular resistance were lower with L500. Although kidney injury and albuminuria were partially reduced by L50 at four months postsurgery, L500 completely arrested kidney inflammation and injury and was associated with regression of albuminuria. This finding suggests that full blockade of angiotensin-I receptors requiring much higher doses of ARBs may be associated with maximum nephroprotection.
Human studies show that ACE inhibitors and ARBs have similar benefits on albuminuria and progression of kidney function loss in both diabetic and nondiabetic kidney disease [18-20]. Any noncomparable effects of ACE inhibitors and ARBs may have resulted from variable blood pressure-lowering efficacy of different ARBs [18,21-23]. In addition, real-world evidence from a large observational study (including approximately two million people) found that there was no difference in efficacy of blood pressure control between ACE inhibitors and ARBs, but ARBs were better tolerated [24]. (See "Antihypertensive therapy and progression of nondiabetic chronic kidney disease in adults".)
Other antihypertensive drugs — Other drugs, such as hydralazine, dihydropyridine calcium channel blockers, diuretics, and beta blockers, have not been shown to reverse intraglomerular hypertension (because they do not produce preferential efferent dilatation) and therefore may be less likely to protect against progressive glomerular injury (figure 1) [5,25]. Hydralazine and the dihydropyridine calcium channel blockers (eg, nifedipine, amlodipine), appear to produce prominent afferent or preglomerular arteriolar dilatation [5,6,26,27]. Decreased resistance at this site will allow more of the systemic pressure to be transmitted to the glomerulus, possibly producing no change or even an elevation in intraglomerular pressure, despite the associated reduction in systemic blood pressure. Increased efferent resistance also may occur, as the drug-induced vasodilatation leads to activation of the renin-angiotensin system. In comparison to nifedipine and amlodipine, nondihydropyridine calcium channel blockers (diltiazem and verapamil) are less potent vasodilators and have been shown to decrease the resistance at the efferent arteriole [6,25,28].
Studies using calcium channel blockers in experimental models of kidney disease have revealed conflicting results [6,26]: some have shown increasing proteinuria (consistent with a rise in intraglomerular pressure) and little protection against glomerulosclerosis [27], while others have shown benefit by mechanisms that may in part be independent of the intraglomerular pressure. (See "Secondary factors and progression of chronic kidney disease".)
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