Identification of Nominal Attributes for Intelligent Classification of Chronic Kidney Disease using Optimization Algorithm

Data mining has been widely used to diagnose diseases from medical data. In this study using chronic kidney disease dataset taken from UCI Machine Learning. The dataset has 25 attributes with 400 samples. With 25 attributes that allow redundant data. Redundant data in datasets can reduce computational efficiency and classification accuracy. To increase accuracy of classification algorithm can be done by reducing dimensions of dataset. Correlation-based Feature Selection (CFS) can quickly identify and filter redundant attributes. However, CFS has disadvantage that selected attribute is not necessarily the best attribute. These weaknesses can be overcome by Binary Particle Swarm Optimization (BPSO). BPSO chooses attributes based on the best fitness value. The purpose of this study is to improve accuracy of Support Vector Machine (SVM) by implementing combination of CFS and BPSO as feature selection. Accuracy of SVM in predicting CKD is 63.75%. Whereas, accuracy of SVM by applying CFS as feature selection is 88.75% and average accuracy of ten execution SVM algorithms by applying a combination of CFS and BPSO as feature selection is 95%. Thus, combination of CFS and BPSO as feature selection on the SVM algorithm can improve results of accuracy in diagnosing CKD by 31.25%.

On Being Better Kidney Doctors: Understanding Trajectories, Probabilities, Predictability, and People

There is evidence that HIV-associated nephropathy (HIVAN) can be prevented and its progression slowed by HAART. More than 20 antiretroviral drugs and drug combinations are available, and life expectancy of HIV-infected individuals is now measured in decades. However, it is likely that more indolent forms of HIVAN remain common in the HAART era, predisposing patients to nephrotoxicity from HAART and related therapies. Indeed, the prevalence of acute renal failure and chronic kidney disease appears to be increasing among HIV-infected patients in the United States [1,2], and kidney disease has emerged as an important predictor of mortality [2,3]. Adverse effects of antiviral treatments should be considered, including their long-term renal toxicity and their role in renal scarring after acute adverse events. In addition, the burden of comorbid chronic kidney disease is likely to increase with ageing of the HIV-infected cohort, continued growth of the epidemic among susceptible minorities and increasing prevalence of HAART-related metabolic abnormalities. In this population of patients, evaluation of renal disorders and prevention of evolution toward chronic renal failure are a crucial challenge. Epidemiology of HIV-associated nephropathy and HIV-related diseases Most epidemiological data on HIVAN generated in the pre-HAART era are based on the US Renal Data System (USRDS). Initial clinical studies indicated that 10% of HIV-1-infected patients appeared to develop renal disease, of which 90% showed clinical and/or pathological features consistent with HIVAN [4,5]. Past postmortem studies also yielded a prevalence of HIVAN ranging between 1% and 15%, depending on the population [6,7]. The prevalence and distribution of HIVAN was associated strongly with African-American ancestry [8,9] as indicated by an USRDS-based report of 3653 patients with end-stage renal disease (ESRD) secondary to HIVAN during 1992 to 1997 [10]. Since the introduction of HAART, national epidemiological data show a reduction of incidence of ESRD associated with HIV-associated renal disease in the United States [11,12] contrasting with the steady increase in HIV/AIDS in the general population [13]. From a mathematical model using available epidemiological data on HIV-infected patients in the USRDS database and the Centers for Disease Control and Prevention data for HIV-seropositive patients, Blower et al.[14] suggested that HAART decreases the incidence of ESRD in patients with HIVAN and the mortality from HIV, with an overall efficacy of 23%. This trend has been attributed, in part, to beneficial effects of HAART, which was commenced in 1996. Preliminary retrospective series or case reports support the efficacy of HAART in improving outcome in HIVAN [15–19]. In a retrospective cohort study, Szczech et al.[20] reported that treatment with protease inhibitors (and prednisone) was associated with a slower decline in renal function in patients with HIVAN or other HIV-1-related renal diseases. Cosgrove et al.[18] reported another retrospective series of 23 patients with HIV-1-related nephropathies, including patients with HIVAN. Patients with HIVAN were treated with HAART and none doubled their serum creatinine. In the non-HAART group, all patients showed a doubling of serum creatinine, two patients died and eight required dialysis. One study [21], retrospectively comparing two cohorts of 102 and 33 patients with biopsy-proven-HIVAN in the pre-HAART and in the HAART eras, respectively, also argues for improvement of renal survival by HAART. However, a recent postmortem-based survey reported that 12% of African-American patients dying of HIV-1 infection have histologically confirmed HIVAN [22]. Even if HAART decreases the incidence of HIVAN in African-Americans, the prevalence of HIVAN may not change because of the improvement in the survival of these patients. The onset of HIVAN could, therefore, just be delayed. Indeed, we have recently reported a patient with biopsy-proven HIVAN despite the lack of any past or present AIDS-defining condition and HAART-controlled HIV-1 infection for at least 2 years [23] Schwartz et al.[1] developed a mathematical model of the dynamics of HIV infection in the ESRD population in order to assess the impact of HAART on the progression of patients with AIDS to the development of ESRD and to predict the prevalence of HIV-related ESRD through to 2020. The authors concluded that, despite the potential benefit of HAART, the prevalence of HIV-related ESRD in the United States would be expected to rise in the future as a result of the expansion of the number with AIDS among black individuals. Nonetheless, while prospective controlled trials evaluating HAART on HIVAN or other HIV-1-related nephropathies are not ethically acceptable, consensus guidelines recommend consideration of HAART in HIV-infected patients with chronic renal insufficiency [24]. Changes in clinicopathological presentation HIV-associated nephropathy HIVAN is an unusual form of poorly responsive glomerular disease characterized by nephrotic syndrome, focal segmental glomerulosclerosis and a rapid fulminant progression to ESRD. Proteinuria occurs in up to 30% of HIV-infected patients, but not all of these patients have HIVAN [25–27]. The true prevalence of HIVAN is not known. The geographic distribution of HIVAN is not uniform, and it depends on specific risk factors for HIV disease, including race, gender and drug use. There is a striking predilection for HIVAN among African-Americans, as is also true for focal segmental glomerulosclerosis associated with intravenous drug use [4]. HIVAN is 7–10 times more common in men than in women, and 30–60% of people with HIVAN have a history of intravenous drug use [7]. In the pre-HAART era, patients with HIVAN typically presented with a nephrotic syndrome consisting of nephrotic-range proteinuria classically without oedema despite severe hypoalbuminaemia. Urinalysis reveals microhaematuria. Patients with HIVAN are typically not hypertensive, even in the face of renal insufficiency, and their kidneys are usually normal to large in size and highly echogenic by ultrasonography. The most common histological light microscopy finding is a collapsing form of focal segmental glomerulosclerosis. Tubulo-interstitial scarring, atrophy and marked dilatation of the tubules (microcystic dilatations) are usually present. Immunofluorescent microscopy is usually negative. Electron microscopy reveals wrinkling of the basement membranes, epithelial cell proliferation and focal foot process effacement. Tubulo-reticular structures in the glomerular endothelial cells consisting of ribonucleoprotein and membrane, the synthesis of which is stimulated by alpha-interferon, is highly predictive of HIVAN. Risk factors for progressive renal disease include CD4 cell count < 200 cells/μl, detectable plasma HIV RNA, hypertension, low plasma albumin and elevated serum creatinine [28]. In our experience during the HAART era, where most patients have well-controlled HIV, a nephropathy typically presents as stable or slowly progressive renal failure, hypertension, glomerular proteinuria, not necessarily of nephrotic range, and a preserved rather than increased kidney size. Pathologically, simple tuft ischaemia tends to replace florid (?) glomerular collapse while mild interstitial infiltration and cystic tubular dilatation are seen. Paradoxically, we noted more frequent atherosclerotic vascular changes even in younger affected patients. Until recently, the clinical course of HIVAN was one of inexorable progression to ESRD in 6–12 months, with limited treatment options. More options are now available to patients; these include antiretroviral therapy, steroid treatment and angiotensin-converting enzyme inhibitors. Evidence exists that antiretroviral therapy can reverse or improve the progression of HIVAN [15,16,19]; however despite the widespread use of HAART, no prospective studies have demonstrated benefit in slowing the progression of HIVAN. The survival benefit from antiretroviral therapy is indisputable. HAART may also prevent the development of HIVAN in at-risk groups. Lucas et al.[29] evaluated a cohort of 3976 at-risk patients in the Johns Hopkins HIV clinic database from 1989 to 2001. They identified 135 cases of HIVAN based on either clinical or pathological criteria. There was a 50% decline in HIVAN incidence in 1998–2001 compared with 1995–1997, and HAART was associated with a 60% reduction in risk for developing HIVAN. Patients with AIDS developed HIVAN at a rate of 12.5/1000 person-years, compared with 3.1/1000 person-years in patients without AIDS (relative risk, 4.1). However, it is notable that in over 1071 person-years of follow-up, no patient developed HIVAN when HAART was initiated prior to the onset of AIDS. The rationale for treating HIVAN with corticosteroids is that steroids are the mainstay of treatment for idiopathic focal segmental glomerulosclerosis [30]. The first report of steroid treatment in four patients with HIVAN found a significant reduction in serum creatinine after a course of corticosteroids lasting 2–4 weeks [31]. The initial case report study has now been extended to include 20 patients, and these results confirm that prednisone at a dose of 60 mg daily for 2–11 weeks leads to a significant reduction in serum creatinine and in 24-hour urinary protein excretion [30]. The encouraging short-term results must be balanced by the findings during the follow-up period. During a median follow-up of 44 weeks, 8 of 20 patients required maintenance dialysis, 11 of 20 died of HIV disease after completing prednisone treatment, and 6 of 20 developed serious infections while receiving prednisone. Only 7 of 20 patients were alive and free from ESRD after a median of 25 weeks following initiation of prednisone. A more recent retrospective study reported the course of HIVAN in 13 patients treated with prednisone and a further eight patients not treated with prednisone. Even after controlling for baseline creatinine, proteinuria, and CD4 cell count, among other variables, the prednisone group had an 80% reduction in risk of progressive azotaemia after 3 months [32]. Prednisone may work by reducing the amount of interstitial inflammation [33]. In 1995, The AIDS Clinical Trials Group (ACTG) designed a phase II randomized, double-blind, placebo-controlled multicentre trial to determine the efficacy of prednisone therapy in HIVAN, but this trial was cancelled because of poor patient recruitment. The angiotensin-converting enzyme inhibitors captopril and fosinopril have also been studied as possible therapy for HIVAN [34]. In one study in which 18 patients were enrolled, nine were treated with captopril, 6.5–25 mg three times daily, and nine controls did not receive captopril. All patients had biopsy-proven HIVAN, and renal survival was defined as the time from initiation of captopril treatment to initiation of dialysis (ESRD). The initial mean serum creatinine concentration was 34 mg/l (±7.0) in the captopril group and 37 mg/l (±0.5) in the controls. A small renal survival advantage of approximately 8 weeks (median 83 versus 30 days), was seen in the captopril group [35]. Two non-randomized studies have investigated the effect of fosinopril on the progression of HIVAN. Both studies showed a significantly lower risk of reaching ESRD in the fosinopril group compared with non-treated controls [35,36]. Despite the limitations of these studies, they suggest that therapy with an angiotensin-converting enzyme inhibitor initiated early may offer renal survival benefits in HIVAN. The ACTG is currently developing a clinical trial (protocol A5179) to compare treatment with an angiotensin receptor blocker (valsartan) plus HAART with HAART alone in patients with HIVAN. Indications for kidney biopsy The decision to obtain a renal biopsy sample is somewhat controversial in the general medical community. Even if a patient presents with the classic clinical features of HIVAN, clinical presentation is predictive of the biopsy diagnosis in only 50–60% of patients. Furthermore, non-invasive tests or clinical markers to identify the precise renal lesion do not exist. Renal biopsy should be offered to patients because a variety of renal lesions occur in HIV-infected patients, and the treatment implications and prognosis vary according to the biopsy results. We, therefore, believe that to distinguish HIVAN from other forms of renal disease, and to redefine HIVAN pathological findings in the HAART era, HIV-positive patients who have unexplained renal abnormalities (i.e., kidney failure and/or daily protein excretion greater than 1 g and/or microscopic haematuria) should have a renal biopsy. HAART-related kidney disorders Electrolyte and acid-base profiles It is noteworthy that the biological profile in HIV-infected patients has dramatically changed in the HAART era. Previous studies stated that hyponatraemia, hyperkalaemia or hypokalaemia and acidosis were the main biological abnormalities in HIV-positive patients [37,38]. A prospective cross-sectional descriptive study (1219 HIV-infected patients over 3 months) undertaken to assess the prevalence of fluid electrolyte and acid–base disturbances showed hyperuricaemia and hypophosphataemia to be the most prevalent abnormalities [39]. Hyperuricaemia was detected in 140 (41.3%) out of the 339 patients tested. Among hyperuricaemic patients, only 47% were treated with didanosine. Multivariate analysis showed that patients not taking non-nucleoside transcriptase inhibitors (NNRTI) had a 1.8-fold risk [95%confidenceinterval(CI),1.1–2.9] of hyperuricaemia. With protease inhibitor treatment and male gender, the risk of hyperuricaemia rose to 4.4 (95% CI, 2.1–9.6). A plasma phosphate level below the normal range was observed in 63 (17.2%) of the patients tested for plasma phosphate. Multivariate analysis showed that patients taking an NNRTI regimen had a 1.9-fold increase in risk of hypophosphataemia (95% CI, 1.1–3.3), male patients had a 2.6-fold increase in risk (95% CI, 1.1–6.3). Bicarbonate plasma level below the normal range was observed in 112 patients (13.6%) out of the 824 patients tested. Multivariate analysis showed that patients taking HAART had a 4.4-fold increase in risk having a low plasma bicarbonate level (95% CI, 2.2–8.9), women had a 2.4-fold increased risk (95% CI, 1.5–3.8) and patients with CD4 cell count < 200 cells/μl had a 1.8-fold increased risk (95% CI, 1.2–2.9). Only 13 patients (3.1%) out of the 419 patients tested exhibited low calcium levels (n = 13). Factors significantly associated with low plasma calcium concentrations were NNRTI regimen and CD4 cell count. An absolute CD4 count < 200 cells/μl was associated with an increased risk of hypocalcaemia when compared with a cont of > 200 cells/μl. Lactic acidosis Approximately 20–30% of patients who are treated with nucleoside reverse transcriptase inhibitors (NRTI) can be found to have asymptomatic hyperlactataemia; this typically develops after several months of therapy and may be transient [40–42]. Severe lactic acidosis is much rarer, occurring in 1.5–2.5% of patients, is usually preceded by fatigue, nausea, vomiting, anorexia, abdominal pain and other systemic symptoms, and is associated with a mortality rate of approximately 80%. Lipoatrophy, myopathy, peripheral neuropathy and pancreatitis are more often observed in patients with symptomatic hyperlactataemia rather than in patients who have frank lactic acidosis. Risk factors include NRTI use, longer duration of treatment, older age, female gender, pregnancy, hypertriglyceridaemia, obesity, concomitant hepatitis C infection, use of ribavirin, impaired kidney function and alcohol ingestion [41–44]. Acute renal failure Before the HAART era, mild acute renal failure, defined as a peak serum creatinine ≥ 20 mg/l, was been reported to occur in up to 20% of hospitalized HIV-infected patients [45]. This is in comparison with an incidence rate of 1% in hospitalized non-HIV-infected patients [46]. The two major acute renal complications in HIV disease that resulted in potentially reversible failure were acute tubular necrosis and HIVAN. Sepsis contributed to the development of severe acute tubular necrosis, defined as a peak creatinine ≥ 60 mg/l, in up to 75% of cases [47]. A study of kidney biopsy specimens in HIV-infected patients with severe acute renal failure not thought to be from prerenal causes or acute tubular necrosis reported the following distribution of renal lesions: 53% haemolytic uraemic syndrome; 40% acute tubular necrosis, either of ischaemic–toxic origin or rhabdomyolysis; 26% obstructive renal failure, extrinsic, drug induced or secondary to paraprotein precipitation; 23% HIVAN; 3% acute interstitial nephritis; and 6% various glomerulonephritides [48]. In a recent cohort study of ambulatory HIV-infected patients, acute renal failure occurred in nearly 10% of patients, with an incidence rate of 5.9 episodes/100 person-years [49] Antiretroviral agents have been shown to have a range of nephrotoxic effects, including crystal-induced obstruction, tubular toxicity, interstitial nephritis and electrolyte abnormalities. Drugs are responsible for one-third of all acute renal failure events. Although only responsible for a few events, antiretroviral drugs cause two-thirds of all obstructive acute renal failure. Indinavir, tenofovir, and nevirapine were the antiretroviral drugs associated with acute renal failure in this cohort [49–52]. Iatrogenic acute renal failure can be dose dependent, manifesting as acute tubular necrosis, acute glomerulopathy, vascular disease or interstitial immunoallergic reactions. Table 1 summarizes the nephrotoxicities induced by antiretroviral drugs [53–77]. According to the renal syndrome, the clinician will attempt to distinguish between possible causes from each of the four aetiopathogenic groups of nephropathies defined above. Depending on the situation, renal biopsy may be indicated. Table 2 proposes a diagnostic flowchart applicable for a HAART- treated patient with renal abnormalities.Table 1: Antiretroviral drug-induced renal abnormalities.Table 2: HIV-infected patients with renal abnormalities: a diagnosis proposition.Chronic renal failure Chronic renal abnormalities are frequently observed in HIV-infected individuals. Despite drug adjustment, some HIV-infected patients experience progressive renal disease. Usually, the diagnosis of renal toxicity of antiretroviral treatment is considered when patients experience acute renal abnormalities. However, the potential insidious long-term renal toxicity of antiviral treatment may be underappreciated in the pathogenesis of nephropathies of chronic progression in HIV infected patients. In prospective studies evaluating the safety and efficacy of the protease inhibitor indinavir, or some reverse transcriptase inhibitors, a of patients with acute renal failure did not their baseline renal function and data the of renal after acute renal related to antiretroviral the large range of kidney diseases that may occur in HIV-positive patients taking HAART, each case should be and the benefits and of drug The main for the clinician is to determine the of the nephropathy in order to specific in to symptomatic complications With the of HIV the complications associated with HIV infection have to include changes in HIV protease inhibitors and the to peripheral and impaired distribution elevated plasma and and elevated plasma have been reported in clinical trials and in changes in may be related to HIV disease or may be a of treatment with antiretroviral agents through in to long-term antiretroviral therapy the development of chronic kidney disease, through metabolic complications Indeed, black and have been associated with the development of Both protease inhibitors and NNRTI have been associated with and studies have shown plasma concentrations to be associated with increased mortality in in and/or older patients Evidence of hyperuricaemia in HIV-positive patients should to change in the of patients, as of The impact of and antiretroviral metabolic disorders on the of kidney or disease in patients with HIV therefore, an important Risk factors for nephrotoxicity renal adverse are not it is possible to identify patients who may be at increased risk factors for kidney disease, including older age, African-American comorbid and kidney disease, to be associated with renal failure in patients In addition, disease and hepatitis have been associated with increased risk for acute or chronic kidney disease in HIV-infected patients kidney function is one of the most of risk for acute or chronic kidney disease in patients The recently consensus guidelines for chronic kidney disease in all HIV-infected patients at the time of with frequent in the of kidney function or other evidence of kidney disease [24]. Initial should include and serum creatinine with of the glomerular rate by either the or of in Renal Disease has been in patients with HIV, are more than serum creatinine of patients with a glomerular rate < 60 will for dose of by the and should more frequent of kidney toxicity and The according to the glomerular rate and the of dose for each are in Table The of proteinuria by or also chronic kidney disease, and may identify patients at increased risk for nephrotoxicity [24]. In to chronic kidney disease, other factors as and concomitant of other nephrotoxic agents may also patients to the nephrotoxic effects of HAART or related HAART can also to Indeed, studies over the past 20 in patient have demonstrated a between in disease and et found a increase in the risk of developing elevated among patients receiving compared with receiving In addition, the results suggested that the increased risk associated with was at least in part, through an increase in Antiretroviral dose based on creatinine with HIV and hepatitis or C The effect of with hepatitis in and C on disease progression and survival among patients infected with HIV has an increasing this has from the effects of while this function and decreases the incidence of infections in HIV-infected patients, it also the of chronic disease to the overall and mortality of these individuals. use of alcohol is an in this Approximately of HIV-infected patients are Among intravenous drug with HIV, this rate is at least 50% and can be up to 90% in with and HIV is with of HIV-infected individuals having evidence of past or infection The prevalence of chronic of among HIV-infected individuals is Among intravenous drug 90% of HIV-infected individuals have evidence of to and 60% also have evidence of past infection with the of of renal disorders has not been reported in However, proteinuria and have been reported frequently in or patients without HIV proteinuria to and in infected patients; proteinuria to 30% and 30% in patients. has been in and patients and is characterized by and peripheral neuropathy The renal presentation of in patients may include renal insufficiency, proteinuria, and The course of renal disease is much more in the with some to ESRD in a of months However, while reports had shown between HIV and with et did not an between HIV infection and In patients not with HIV, the of nephropathy with and has also been and the reports of nephropathy in HIV-infected patients may be by the incidence of infection, and in this population The life expectancy of HIV-positive patients treated with HAART now that of the general The has to the and renal that can increase with more in patients hypertensive, 2 and risk factors to renal disorders from HIV infection and HAART. it more important to develop for treating these patients from the renal Renal to be in patients with HIV/AIDS and potentially reversible factors to be identified and the we suggest the antiretroviral drug use and kidney disease in HIV-infected patients. All patients at the time of HIV diagnosis should be for kidney disease with a for proteinuria and a of renal is no evidence of proteinuria at initial patients at risk for the development of renal disease (i.e., African-Americans, with CD4 cell < 200 cells/μl or plasma HIV > and with hypertension, or should Renal function should be on a to assess for changes over proteinuria, renal renal biopsy. Patients with glomerular rate 60 or with proteinuria > by or on should be to a for further evaluation and In HIV-infected patients with evidence of should be controlled to a level no than enzyme inhibitors or angiotensin receptor are the drugs of first for patients with proteinuria, and these drugs should also be considered in HIV-infected patients with renal disease. should be in patients receiving protease inhibitors. Patients with HIVAN should be treated with HAART at HAART should not be from patients because of the of their renal The antiretroviral regimen is a between the benefits of and the risk of adverse events, including The of renal insufficiency should the and dose of the antiretroviral of prednisone should be considered in patients with HIVAN if HAART alone not result in improvement of renal function or in patients with HIVAN renal failure is A that the of short-term the benefit of slowing the progression to ESRD and the should the decision reduction of for antiretroviral drugs that are the kidneys is With dose and renal insufficiency or ESRD is not an absolute to the use of any antiretroviral nucleoside should not be in patients with renal function for of the development of lactic acidosis. Drugs that are by dialysis should be after to of In HIV-positive renal are important between the inhibitors and protease inhibitors, and the NNRTI drug may increase levels of and tenofovir, their In the of protease inhibitors, a major reduction in the of inhibitors may be Although most antiretroviral agents are free of renal toxicity, renal can occur and may to be from progression of HIVAN or other HIV-related kidney kidney diseases by other infections or or kidney diseases to HIV infection and its and diseases have emerged as important complications in patients, infections as causes of among HIV-infected patients. patients with risk or a history of a consideration should be to or to protease antiretroviral with the use of NRTI or NRTI and and between disease and will diagnosis and treatment of chronic kidney and vascular diseases with the of progression to ESRD. The authors and for their The authors in the had to all the data in the study and had for the decision to to

The Impact of APOL1 on Chronic Kidney Disease and Hypertension.

The two leading causes of chronic kidney disease (CKD) are excessive blood pressure and diabetes. Researchers worldwide utilize the rate of globular filtration and kidney inflammation biomarkers to identify chronic kidney disease that gradually reduces renal function. The mortality rate for CKD is high, and thus, a person with this illness is more likely to pass away at a younger age. Healthcare professionals must diagnose the various illnesses connected to this deadly disease as promptly as possible to lighten the impact of CKD. A quantum machine learning (QML) based technique is presented in this research to help with the early diagnosis and prognosis of CKD. The proposed research comprises four phases: data pre-processing, data augmentation, feature selection, and classification. In the first phase, Kalman filter and data normalization techniques are applied to handle the missing and noisy data. In the second phase, data augmentation uses sparse autoencoders to balance the data for smaller classes. In the third phase, LASSO shrinkage is used to select the significant features in the dataset. Variational Quantum classifiers, a supervised QML technique, are employed in the classification phase to classify chronic kidney diseases. The proposed system has been evaluated on the UCI dataset, which comprises 400 CKD patients in the early stages with 25 attributes. The suggested system was assessed using F1-score, precision, recall, and accuracy as evaluation metrics. With a 99.2% classification accuracy, it was found that this model performed better than the other traditional classifiers used for chronic kidney disease classification.

Chronic kidney disease as a global public health problem: Approaches and initiatives – a position statement from Kidney Disease Improving Global Outcomes

Chronic kidney disease (CKD) can be treated if it is detected early, but as the disease progresses, recovery becomes impossible. Eventually, renal replacement therapy such as transplantation or dialysis is necessary. Ultrasound is a test method with which to diagnose kidney cancer, inflammatory disease, nodular disease, chronic kidney disease, etc. It is used to determine the degree of inflammation using information such as the kidney size and internal echo characteristics. The degree of the progression of chronic kidney disease in the current clinical trial is based on the value of the glomerular filtration rate. However, changes in the degree of inflammation and disease can even be observed with ultrasound. In this study, from a total of 741 images, 251 normal kidney images, 328 mild and moderate CKD images, and 162 severe CKD images were tested. In order to diagnose CKD in clinical practice, three ROIs were set: the cortex of the kidney, the boundary between the cortex and medulla, and the medulla, which are areas examined to obtain information from ultrasound images. Parameters were extracted from each ROI using the GLCM algorithm, which is widely used in ultrasound image analysis. When each parameter was extracted from the three areas, a total of 57 GLCM parameters were extracted. Finally, a total of 58 parameters were used by adding information on the size of the kidney, which is important for the diagnosis of chronic kidney disease. The artificial neural network (ANN) was composed of 58 input parameters, 10 hidden layers, and 3 output layers (normal, mild and moderate CKD, and severe CKD). Using the ANN model, the final classification rate was 95.4%, the epoch needed for training was 38 times, and the misclassification rate was 4.6%.

Background and Aims Chronic kidney disease (CKD) is often a silent condition, with symptoms typically not appearing until a large proportion of kidney function has been lost. Therapeutic interventions, e.g., disease-modifying medications, blood pressure and diabetes control, and lifestyle changes, can delay CKD progression, particularly if instigated early. However, psychological distress can reduce adherence to interventions. It is important patients are adequately informed about their diagnosis to improve adherence and reduce the impact of distress. Multinational, real-world data on patient experiences with CKD, particularly about clinical management, treatment patterns and quality of life, are limited. This DISCOVER CKD sub-study aimed to capture the emotions elicited by patients at CKD diagnosis and their perceptions of the information received. Method DISCOVER CKD (NCT04034992) is a multinational cohort study that aims tocharacterise the epidemiology of CKD and describe patient characteristics, CKD progression, clinical outcomes, the patient journey, practice patterns, and clinical management. The current analysis includes a subset of patients from the USA, UK, Japan, and Spain, who participated in 1-2-1 telephone interviews about their CKD experience, including their disease journey and interactions with the healthcare system. Interview topics in DISCOVER CKD were informed by a pilot study that utilised data from PatientsLikeMe, an online network for patients to share personal stories and health data. Qualitative interviews, conducted in the local language by trained interviewers, January–June 2023, lasted ∼60–90 minutes. Transcribed interviews were translated into English for coding (MAXQDA Plus 2022 v22.3.0) and analysis. The study received research ethics board approval and all participants provided written informed consent. Results 103 patients (mean age 63.1 years; 42.7% female; 51.5% with type 2 diabetes) were interviewed. Most had CKD stage 3A (22.3%) or 3B (28.2%); 26.2% had stage 4 or 5 no dialysis and 9.7% were stage 4 (n = 1) or 5 on dialysis. Average time since diagnosis was 9.5 years. Over one-third (38.8%; n = 40/103) of participants did not recall any specific symptoms or signs of CKD prior to diagnosis. Of the pre-diagnosis symptoms reported, the most common was fatigue (21.4%; n = 22/103), then high blood pressure (15.5%; n = 16/103) and swelling (11.7%; n = 12/103). With respect to patient experiences, 55.2% (n = 32/58) said they did not feel sufficient information about CKD was provided at diagnosis and 59.2% (n = 45/76) said no information about their CKD stage was shared. Participants felt overwhelmed and confused about the diagnostic process and struggled to understand the information provided to them, including information about kidney function and symptoms. To supplement their understanding, participants reported using additional sources of information, including the internet (52.9%; n = 36/68), other healthcare professionals (HCPs) (19.1%; n = 13/68), books/printed information (11.8%; n = 8/68) and patient support groups (8.8%; n = 6/68). The most common emotions experienced at the time of diagnosis were worry and fear (28.2%; n = 29/103), then shock/surprise (25.2%; n = 26/103) (Figure). For those reporting no reaction (27.2%; n = 28/103), many stated the condition had no discernible effect on their daily lives. Reasons for fear or worry were related to the potential for disease progression. Conclusion Many patients expressed dissatisfaction with the information they received at their CKD diagnosis. This suggests that HCPs could dedicate more time to explaining the diagnosis, the characteristics and severity of CKD, likelihood of progression, and the benefits of self-management and adherence to intervention. This could be particularly important for those without symptoms at the time of diagnosis, and patients who rely on HCPs as their primary source of information. Patients should be asked what information they want to receive and be directed to trusted sources. The diagnostic process was a highly emotional experience for many patients and counselling or psychological therapy should be considered.

Leveraging the Electronic Health Record to Optimize Chronic Kidney Disease Care

THE TERM CHRONIC KIDNEY DISEASE(CKD)WAS FIRST PROposedandsystematicallydefinedin2002,andthe5incrementalstages for thedegreeofseverityofCKDwere describedbasedontheestimatedglomerular filtration rate (GFR) (stage 1, 90; stage 2, 60-89; stage 3, 30-59; stage 4,15-29;andstage5, 15mL/min/1.73m).Stage1 is the least severeandstage5isclassifiedaskidneyfailure. Theestimated GFR (calculated from the Modification of Diet in Renal Disease [MDRD] Study equation) can be derived automatically from a single serum creatinine measurement, combined with theeasilyavailableageandsexdata,plusaqualifyingstatement on race, and without a need for patient weight. The automated estimated GFR calculation has rapidly becomearoutinecomponentofvirtually every laboratory report ofserumcreatinineconcentration.Thishasoccurredeventhough estimated GFR is not based on an accurate timed urine specimen, is only a rough estimate of a patient’s actual GFR, and is more applicable to the population than to the individual. An estimatedGFRlowerthan60mL /min/1.73m hasbeenflagged asindicatingmoderatetoseverekidneydisease andphysicians, followingtheguidelines,sometimesinformpatientsofthisfinding. The prevalence of CKD using the MDRD equation in nationally representative surveys has been estimated at 10% to 12% of the population, with CKD stage 3 (estimated GFR 3059mL/min/1.73m)comprisingthelargestcategory.Populationbasedstudieshaveconsistentlyreportedastrongandincremental association between CKD stages and risk of cardiovascular events and death, suggesting that an individual with low estimated GFR (ie, stage 3, 4, or 5) might be at increased risk. The use of the term “kidney” along with the new CKD staging and its expanded spectrum based on estimated GFR of less than 60 mL /min/1.73 m has increased awareness about and the apparent prevalence of a once underappreciated and confusingdisease state. Consequently,nephrologistshavehadan unprecedented increase in consultations to verify the diagnosis of “CKD stage 3 ” primarily because of a calculated estimatedGFRoflessthan60mL /min/1.73m.Manypatientswith thisallegeddiagnosisareanxiousuntil theyseeanephrologist, whereas thespecialist feels compelled,perhaps inpartbecause of concerns of litigation, to perform extensive and expensive workupstomoreaccuratelyassessrenal function.Someofthese patients have been stigmatized with a “preexisting condition” andhavebeendeniedinsurancecoverageuponreemployment. However, the diagnosis of stage 3 CKD for many patients cannot be substantiated other than with an estimated GFR of less than 60 mL /min/1.73 m according to the MDRD equation. Nephrologists have not adequately addressed the clinical and public health consequences of using the MDRD equation as a criterion for the detection and classification of CKD and have failed to acknowledge the many implications of the flaws in this approach. For instance, it is counterintuitive that more patients are classified as having stage 3 of a chronic disease than earlier stages, ie, stage 1 and 2 combined, in sharp contradistinction to other chronic disease states such as heart failure. The result has been that the nephrology community appears to have undermined its own important work in public health by overdiagnosing a nonexistent disease in millions of elderly persons as well as in women in whom the MDRD equation calculates a 25% worse kidney function by default, or in adults with larger muscle mass or other nutritional states associated with higher serum creatinine independent of kidney function. Use of the epidemiological classification of such an imperfect surrogate as estimated GFR does not square with the clinical reality of patient diagnosis and treatment. Many patients with so-called CKD stage 3 do not die of renal causes, and do not develop end-stage kidney disease over time, so there is a disconnect between classification based on estimated GFR equations and patients’ clinical course. At the same time, the diagnosis of true kidney disease may be missed in some persons with lower serum creatinine levels due to smaller skeletal muscle mass, low or no protein intake, or significant glomerular, tubular, or vascular kidney disease but with higher estimated GFR. As a result, and despite the overwhelming data on the association of kidney disease with cardiovascular events and death, the cardiology community has generally not considered CKD based on estimated GFR alone as a credible cardiovascular risk fac-

Chronic kidney disease (CKD) is a global health burden that affects approximately 10% of the adult population in the world. It is also recognized as the top 20 causes of death worldwide. Unfortunately, there is no cure for CKD however, it is possible to slow down its progression and mollify the damage by early diagnosis of the disease. Due to a limited number of nephrologists, the early diagnosis of CKD is often not possible for most of the people. Therefore the use of modern computer-aided methods is necessary to aid the traditional CKD diagnosis system to be more efficient and accurate. In this research, our primary focus was to apply 3 modern machine learning techniques namely logistic regression, feedforward neural networks and wide & deep learning to diagnose CKD as well as finding the best performing technique by evaluating their diagnosis performance. To evaluate their performance, f1-score, precision, recall and AUC score was used for logistic regression and an additional loss score was considered for the feedforward neural networks and wide & deep model. We found the feedforward neural network as the best performing technique for CKD diagnosis with 0.99 f1-score, 0.97 precision, 0.99 recall and 0.99 AUC score. Logistic regression produced the lowest result among all and the wide & deep learning with a larger number of hidden layers and neurons found to be effective for larger datasets.

GFR is the accepted metric for evaluating renal function but measuring it directly (mGFR) can be cumbersome, time-consuming, and costly. The constant infusion method using inulin as the filtration marker, introduced in 1934 by Richards and Smith (1), has undergone many revisions that have now made mGFR easier to perform, although not widely available (2,3). A simple, reliable, unbiased, precise, and accurate estimation of mGFR, without reliance on constant infusions or timed urinary collections, would be welcome; however, as illustrated by the extensive compendium of comparisons of mGFR (using classical inulin clearance methods) to eGFR by Botev et al. (4) in this issue of CJASN , this objective is far from being realized. Although formulaic methods to approximate the values of mGFR from serum creatinine (Scr) levels have been used for many decades, the seminal description of the Modification of Diet in Renal Disease (MDRD) equation (eGFR-MDRD) in 1999 galvanized interest in this common and important clinical issue (5). The often used Cockcroft-Gault equation (6) was never intended to be an approximation of GFR but rather was designed to estimate endogenous creatinine clearance, which is not equivalent to GFR because of the effects of tubular secretion of creatinine (TScr). In normal individuals, this can be compensated for by a correction factor, because TScr is relatively constant (at approximately 22 to 24% of GFR) (7); however, TScr can vary markedly in disease states, particularly those associated with heavy proteinuria (8). Compared with mGFR, the current widely used eGFR-MDRD formulas (original and reexpressed [5,9]) have limitations because of variable degrees of bias, imprecision, and inaccuracy (10). The studies of Botev et al. (4) in this issue of CJASN provide additional quantitative data on the ranges of bias, precision, and accuracy of eGFR-MDRD according to the levels …

Longitudinal studies evaluating the association between visceral fat area (VFA) and kidney function decline in patients with chronic kidney disease (CKD) are limited, and little is known about VFA interactions contributing to the kidney prognosis (e.g. interactions between VFA ≥ 100cm2 and age, sex, and CKD category). In this study, we stratified patients with CKD according to VFA category, as well as age, sex, CKD category, hyperglycemia, and diabetes mellitus, and determined the ability of obesity-related indicators (body mass index, waist circumference, subcutaneous fat area, visceral-to-subcutaneous fat ratio) to predict the renal prognosis. Kidney outcomes (≥ 50% estimated glomerular filtration rate decline or end-stage kidney disease) were examined in 200 patients with CKD (median follow-up, 12.3years). On multivariable Cox analysis, an increase in VFA (10-cm2 increase) was significantly associated with kidney outcomes in the entire cohort, and VFA was significantly associated with kidney disease progression even in the VFA < 100cm2 sub-cohort. Interestingly, the hazard ratio (HR) was higher for VFA (10-cm2 increase) than for the VFA ≥ 100cm2 sub-cohort (HR 1.33 vs. 1.07). Overall, VFA was found to be the most versatile obesity-related indicator associated with kidney disease progression. VFA was associated with the primary outcome in the sub-cohorts of CKD stages 1-2, hyperglycemia, and diabetes mellitus. A high VFA was a significant kidney prognostic factor in the entire CKD cohort, with greater significance in patients with VFA < 100cm2 than in patients with VFA ≥ 100cm2. Our results may provide new insights into strategies for treating CKD.

Blood Pressure Goals: How Low Is Safe in CKD?

The Third World Kidney Day: Looking Back and Thinking Forward