Chronic Kidney Disease: A Guide

Written By Danial Mirza

Definition

Chronic Kidney Disease (CKD) is formally defined as the presence of abnormalities in kidney structure or function, which persist for more than three months and carry tangible implications for an individual's health (4, 12). This definition is intentionally broad to encompass the wide spectrum of disorders that can lead to chronic renal impairment. It is crucial to understand that "CKD" is not a single diagnosis but a powerful classification framework. It identifies a population of patients who are at significant risk for two major adverse outcomes: the progressive and irreversible loss of kidney function leading towards end-stage renal disease (ESRD), and a dramatically increased risk of cardiovascular disease and mortality (1). Therefore, a diagnosis of CKD is a call to action, mandating a thorough evaluation to determine the underlying cause and the implementation of strategies to mitigate these risks.

The diagnosis requires meeting at least one of two core criteria for a duration exceeding three months, a temporal element essential for distinguishing chronic, irreversible processes from acute, potentially reversible kidney insults like Acute Kidney Injury (AKI) (1, 9).

Epidemiology

Chronic Kidney Disease represents a significant and escalating public health crisis in Malaysia. National data reveals a stark reality: the prevalence among Malaysian adults surged alarmingly from 9.1% in 2011 to 15.5% in 2018, which translates to over five million individuals living with the condition (20, 56). The vast majority of these cases are in the early, asymptomatic stages. This creates a "silent epidemic," compounded by a profound lack of awareness; it is estimated that up to 90% of individuals with CKD in Malaysia are unaware of their diagnosis (57). This silent majority, often feeling perfectly well, represents a massive, undiagnosed reservoir of disease that is quietly progressing towards more advanced stages, highlighting a critical gap in public health education and systematic screening programs. This epidemic is primarily fueled by the high and rising prevalence of its two main drivers: Type 2 diabetes and hypertension (22).

Globally, CKD is a pandemic, affecting an estimated 11-13% of the world's population (6). The burden is particularly severe in Southeast Asia, where diabetic kidney disease is the leading cause of ESRD (52). Malaysia's situation is especially dire, as the nation has one of the highest incidence rates of treated ESRD in the world. Projections indicate that if current trends are not curbed, over 106,000 Malaysians will require life-sustaining dialysis by the year 2040 (22, 56). This places an economically unsustainable burden on the healthcare system, consuming a disproportionate share of the national health budget and threatening future capacity to provide care.

Pathophysiology

Regardless of the initial insult—be it the metabolic stress of diabetes, the barotrauma of hypertension, or an autoimmune attack—the progression of CKD often converges on a final common pathway. This pathway is characterized by a relentless, self-perpetuating cycle of nephron loss (24). When an initial disease process irreversibly destroys a subset of nephrons, the remaining healthy nephrons are forced to compensate to maintain overall kidney function. They undergo hypertrophy and increase their individual filtration rate, a phenomenon known as single-nephron hyperfiltration. While this is a remarkable short-term adaptation, it becomes maladaptive over the long term. The increased workload leads to elevated pressure within the delicate glomerular capillaries (intraglomerular hypertension), causing mechanical stress, direct injury to the specialized podocyte cells that form the filtration barrier, and eventual scarring of the glomerulus (glomerulosclerosis) (24).

The Renin-Angiotensin-Aldosterone System (RAAS) is a central mediator of this damaging process. In response to perceived under-perfusion, RAAS activation leads to the generation of Angiotensin II, which preferentially constricts the efferent arteriole (the vessel exiting the glomerulus). This action acutely preserves filtration but chronically exacerbates the damaging intraglomerular hypertension. Furthermore, Angiotensin II has direct non-hemodynamic effects, acting as a pro-inflammatory and pro-fibrotic cytokine that stimulates the production of scar tissue, directly promoting renal fibrosis (24).

This damage to the glomerular filtration barrier results in the leakage of albumin into the urine (albuminuria). Albuminuria is not merely a passive marker of damage; it is an active mediator of further injury. The excess filtered protein is reabsorbed by renal tubular cells, a process that is directly toxic. This triggers intracellular inflammatory cascades, leading to tubular cell injury, apoptosis, and the release of signals that recruit inflammatory cells. This incites a local inflammatory response in the surrounding tissue, driving tubulointerstitial fibrosis, which is the strongest histological predictor of a patient's rate of progression towards kidney failure (9, 31).

Clinical Presentation

A defining and challenging characteristic of CKD is its insidious nature. Early stages (G1-G2) are almost always asymptomatic, as the kidney's vast functional reserve can compensate for significant nephron loss without producing noticeable symptoms. Consequently, diagnosis in these stages is rarely prompted by patient complaints and relies almost exclusively on opportunistic screening of at-risk individuals (18, 70).

Diagnostic Clues:

  • Foamy Urine: A sign often reported by patients themselves. The foam is caused by the surfactant properties of excess protein (albumin) in the urine and is highly suggestive of significant albuminuria (69).

  • Red Blood Cell (RBC) Casts in Urine: The presence of these cylindrical structures, which are formed when red blood cells are compressed within the renal tubules, on urine microscopy is pathognomonic for an underlying glomerulonephritis, indicating bleeding from within the glomerulus itself (10).

Common Symptoms (often vague, non-specific, and appearing in Stage 3 onwards):

  • Fatigue, lassitude, and profound weakness, which are compounded by the development of anemia of CKD (69).

  • Hypertension, which is both a cause and a consequence, is present in over 80% of patients with advanced CKD due to fluid retention and RAAS activation (5).

  • Dependent pitting edema (swelling in the feet and ankles) and periorbital puffiness, caused by sodium and water retention (18).

  • Nocturia (the need to urinate frequently at night) is an early symptom resulting from the kidney's loss of its ability to concentrate urine (70).

  • Pruritus (itching), which can be severe, generalized, and distressing, is a hallmark of advanced uremia (70).

  • Anorexia (loss of appetite), nausea, and a persistent unpleasant or metallic taste in the mouth (dysgeusia) are common gastrointestinal symptoms of uremia (74, 71).

⚠️ Red Flag Signs & Symptoms (Indicating advanced disease/uremia and requiring urgent action):

  • Pericardial friction rub: A triphasic, scratching sound heard on cardiac auscultation, suggesting uremic pericarditis. This is a life-threatening condition due to the risk of cardiac tamponade and is an absolute indication for emergency dialysis (37).

  • Asterixis ("flapping" tremor): A coarse, flapping tremor of the outstretched hands, indicating severe uremic encephalopathy and risk of progression to seizures and coma (35).

  • Kussmaul breathing: Deep, labored, sighing respirations as the body attempts to compensate for severe metabolic acidosis by blowing off carbon dioxide (70).

  • Pulmonary edema: Acute shortness of breath, often with frothy sputum, indicating severe fluid overload that has overwhelmed the heart's ability to pump effectively.

Complications

The progressive loss of the kidneys' excretory, metabolic, and endocrine functions leads to a host of multisystem complications that define the clinical syndrome of advanced CKD.

  • Cardiovascular: Hypertension, Left Ventricular Hypertrophy (LVH) from chronic pressure and volume overload, accelerated atherosclerosis, and a unique form of vascular calcification driven by mineral abnormalities. Cardiovascular disease is the leading cause of death in CKD patients, with most dying from a cardiac event before ever needing dialysis (21, 41).

  • Hematological: Anemia of CKD is near-universal in advanced stages. It is primarily caused by deficient production of the hormone erythropoietin by the failing kidneys, but is compounded by functional iron deficiency and a shortened lifespan of red blood cells in the uremic environment (91).

  • Metabolic:

    • CKD-Mineral and Bone Disorder (CKD-MBD): A systemic disorder involving complex dysregulation of serum calcium, phosphorus, parathyroid hormone (PTH), and Vitamin D. This leads to renal osteodystrophy (a form of bone disease) and is a major driver of the extensive vascular and valvular calcification seen in CKD patients (92).

    • Metabolic Acidosis: Due to the impaired ability of the kidneys to excrete the daily metabolic acid load, leading to a state of chronic acidosis that contributes to muscle wasting and bone resorption (93).

    • Hyperkalemia: Impaired potassium excretion creates a high risk of life-threatening high potassium levels, especially with certain medications or dietary indiscretion.

  • Neurological: Uremic encephalopathy (ranging from mild cognitive "brain fog" to confusion, seizures, and coma), a stocking-glove peripheral neuropathy, and restless legs syndrome are common in advanced disease (35, 74).

Prognosis

The prognosis of CKD is highly variable and depends critically on the underlying cause, the GFR stage at diagnosis, the severity of albuminuria, and the effective management of comorbidities. The combination of GFR and albuminuria categories, as visualized in the KDIGO "heat map," provides a powerful and essential tool for predicting the risk of progression to ESRD, acute kidney injury (AKI), and mortality (1). For instance, a patient in the "red" zone has a very high annual risk of progression compared to a patient in the "green" zone. Diabetic kidney disease generally carries a worse prognosis than many other causes. However, early detection and the aggressive implementation of modern reno-protective therapies can significantly slow the rate of GFR decline and improve outcomes.

Differential Diagnosis

When a patient presents with features of CKD, it is crucial to differentiate the underlying cause, as this guides specific management and prognosis. The top differentials are considered narratively:

  • Diabetic Kidney Disease (DKD): This is the leading differential in any patient with a background of diabetes mellitus, especially if accompanied by significant albuminuria. The diagnosis is often clinical, supported by a history of long-standing or poorly controlled diabetes and the presence of other microvascular complications like diabetic retinopathy. The absence of retinopathy in a patient with Type 1 diabetes and kidney disease should prompt a search for an alternative diagnosis (54).

  • Hypertensive Nephrosclerosis: This should be considered in patients with a long history of poorly controlled hypertension. It typically presents with a slower, more indolent rate of GFR decline and less severe albuminuria compared to DKD or active glomerulonephritis. It is often a diagnosis of exclusion after other, more specific causes have been ruled out (64).

  • Primary Glomerulonephritis (e.g., IgA Nephropathy, Lupus Nephritis): This should be a key differential, particularly in younger patients presenting with hematuria (visible or microscopic) and significant proteinuria. The presence of dysmorphic red cells and, most importantly, red blood cell casts in the urine sediment is highly suggestive and points away from DKD or hypertensive nephrosclerosis, warranting urgent nephrology referral for consideration of a renal biopsy (10).

  • Obstructive Uropathy: This is a critical and potentially reversible cause of kidney injury. It must be considered in older men with symptoms of benign prostatic hyperplasia (BPH), or in any patient with a history of kidney stones, pelvic malignancy, or neurogenic bladder. A renal ultrasound is the essential first imaging step to rule out hydronephrosis, which would confirm obstruction (14).

Investigations

Investigations are structured logically to confirm the diagnosis and chronicity, accurately stage the disease, determine the underlying etiology, and monitor for the development of complications.

Immediate & Bedside Tests

  • Urine Dipstick (UFEME): An essential first step in any medical workup to rapidly screen for proteinuria and hematuria. However, an integrated justification is that the protein pad on a standard dipstick is insensitive for detecting moderately increased albuminuria (A2 category), making it an inadequate tool for the early detection of diabetic kidney disease; therefore, a quantitative Urine Albumin-to-Creatinine Ratio is the superior and recommended test (86).

  • Bedside ECG: This is mandatory in any CKD patient presenting with acute illness, weakness, or palpitations, and especially in those with suspected hyperkalemia or uremic symptoms. It is performed to immediately rule out life-threatening arrhythmias (e.g., peaked T waves, sine wave pattern) or signs of pericarditis (e.g., widespread concave ST elevation) (the action), which are fatal complications of advanced CKD that require immediate intervention (the rationale).

Diagnostic Workup

  • First-Line Investigations:

    • Serum Creatinine with calculated eGFR (CKD-EPI formula): This is the fundamental blood test to assess and quantify kidney function. An eGFR, which accounts for age, sex, and race, provides a much more accurate measure of filtration than the serum creatinine level alone (the rationale), allowing for correct staging and risk stratification which guides all subsequent management decisions (the action) (2).

    • Urine Albumin-to-Creatinine Ratio (UACR): This is the recommended gold-standard test for detecting and quantifying proteinuria from a simple spot urine sample. It is highly sensitive for detecting early kidney damage, often years before GFR begins to decline, especially in diabetes (the rationale), and its reduction is a key target for therapy and a powerful predictor of both renal and cardiovascular outcomes (the action) (4).

  • Gold Standard:

    • Renal Biopsy: This is the definitive gold standard for diagnosing most primary glomerular and tubulointerstitial diseases. It provides a precise histological diagnosis (the rationale), which is absolutely essential for guiding specific and often potent immunosuppressive therapy and for providing an accurate prognosis (the action) (15).

Monitoring & Staging:

  • Renal Ultrasound: This is a mandatory, non-invasive imaging study for virtually all new CKD patients. It is performed to assess kidney size, echotexture, and cortical thickness, which helps determine the chronicity of the disease (small, echogenic kidneys suggest long-standing disease) (the action), and to definitively rule out structural causes like bilateral hydronephrosis from obstruction (the rationale) (2, 14).

  • Targeted Serology: A panel including an autoimmune screen (ANA, C3/C4), vasculitis screen (ANCA), and viral markers (Hepatitis B/C, HIV) is performed not routinely, but specifically when a glomerular disease is suspected based on clinical features (e.g., young patient, active urine sediment). This is done to identify the specific underlying cause (the action), as the results will direct urgent and highly specific treatment protocols (the rationale) (15).

Management

Management Principles

The modern management of CKD is a proactive, multifaceted, and long-term endeavor. The primary goals are to aggressively treat the underlying cause where possible, to slow the rate of progressive GFR decline using evidence-based therapies, to actively manage the associated systemic complications, to reduce the exceptionally high burden of cardiovascular disease, and to prepare patients for renal replacement therapy or a conservative care pathway while preserving the best possible quality of life (3).

Acute Stabilisation (The First Hour)

For patients presenting with acute, life-threatening complications of CKD:

  • Airway/Breathing: Administer high-flow oxygen via a non-rebreather mask with the goal of maintaining SpO2 >94% (the action). This is crucial to prevent tissue hypoxia that may be severely exacerbated by co-existing severe anemia or acute pulmonary edema (the rationale).

  • Circulation: For severe fluid overload with frank pulmonary edema, administer a bolus of IV Furosemide 40-80mg (or higher, depending on baseline renal function and diuretic use) (the action) to promote rapid diuresis, reduce cardiac preload, and relieve respiratory distress (the rationale). For severe, uncontrolled hypertension, use parenteral agents like IV labetalol or a GTN infusion for controlled reduction.

  • Disability: Always check a capillary blood glucose to rule out hypoglycemia as a cause for altered mental status. If the patient has confusion, drowsiness, or asterixis, uremic encephalopathy is a primary diagnosis and an urgent indication for nephrology consultation.

  • Exposure/Electrolytes: For severe hyperkalemia (K+ >6.5 mmol/L) or any level with associated ECG changes, immediately administer IV Calcium Gluconate 10ml of 10% solution over 10 minutes (the action). This does not lower potassium but immediately stabilizes the cardiac membrane to prevent fatal arrhythmia (the rationale). This must be followed by measures to shift potassium intracellularly (e.g., Insulin/Dextrose infusion) and definitive measures to remove it from the body (e.g., dialysis).

Definitive Therapy

The modern approach to slowing CKD progression is built on a multi-pillar pharmacological strategy designed to maximize reno- and cardio-protection by targeting different pathophysiological pathways.

  • First-Line Treatment (The Four Pillars):

    1. Blood Pressure & Lipid Control: The target BP is typically <130/80 mmHg according to Malaysian CPGs (2). High-intensity statins are recommended for most CKD patients, regardless of LDL level, for primary and secondary cardiovascular risk reduction.

    2. RAAS Inhibition: Use an ACE inhibitor (e.g., Perindopril 2-8mg OD) or an ARB (e.g., Losartan 25-100mg OD) as foundational therapy in all patients with significant albuminuria (A2/A3). This is essential to reduce intraglomerular pressure and proteinuria by dilating the efferent arteriole (the rationale), which is a cornerstone of slowing CKD progression (the action) (2). It is critical to never combine an ACEi and an ARB due to the risk of adverse events.

    3. SGLT2 Inhibition: Use an SGLT2 inhibitor (e.g., Dapagliflozin 10mg OD, Empagliflozin 10mg OD) for patients with T2D and CKD, and now also for many non-diabetic CKD patients with albuminuria or heart failure. This is vital to reduce intraglomerular pressure via afferent arteriolar vasoconstriction, thereby restoring tubuloglomerular feedback (the rationale), providing powerful, proven benefits in slowing GFR decline and reducing cardiovascular events and hospitalization for heart failure (the action) (90).

    4. Non-steroidal MRA: Consider Finerenone for patients with T2D and persistent albuminuria despite a maximally tolerated dose of a RAAS inhibitor. This is done to provide additional anti-inflammatory and anti-fibrotic effects by blocking aldosterone (the rationale), which further reduces the residual risk of renal and cardiovascular progression (the action) (90).

  • Management of Complications:

    • Anemia: The first step is to assess and replete iron stores, as functional iron deficiency is common. If Hb remains low (<10 g/dL) despite adequate iron, initiate an Erythropoiesis-Stimulating Agent (ESA) to improve symptoms and reduce the need for transfusions (the action), aiming for a target Hb of 10-11.5 g/dL to avoid the increased cardiovascular risk associated with targeting normal hemoglobin levels (the rationale) (91).

    • CKD-MBD: This complex disorder is managed with a three-pronged approach: dietary phosphate restriction, the use of oral phosphate binders (e.g., Calcium Carbonate, Sevelamer) taken with meals, and the use of active Vitamin D sterols (e.g., Calcitriol) or calcimimetics to control secondary hyperparathyroidism. This is done to control serum phosphate and PTH levels (the action), which is crucial for preventing debilitating bone disease and mitigating the risk of vascular calcification (the rationale) (92).

    • Metabolic Acidosis: Treat with oral sodium bicarbonate tablets with the goal of maintaining the serum bicarbonate level at or above 22 mmol/L (the action). Correcting acidosis has been shown to slow CKD progression, improve nutritional status by reducing protein catabolism, and mitigate adverse effects on bone (the rationale) (93).

Key Nursing & Monitoring Instructions

  • Strict hourly input/output chart monitoring for any acutely ill patient to assess fluid balance and renal response to therapies.

  • Monitor blood pressure every 4 hours, or more frequently if the patient is on IV antihypertensives or is hemodynamically unstable.

  • Inform medical staff immediately if systolic BP drops below 100 mmHg, urine output is <0.5mL/kg/hr for more than two hours, or the patient develops new chest pain, shortness of breath, or a change in neurological status.

  • Accurate daily weight monitoring, preferably at the same time each day, is the most reliable method to assess day-to-day changes in fluid status.

Long-Term Plan & Patient Education

The long-term plan involves regular, risk-stratified follow-up to monitor eGFR and UACR, with the frequency determined by the KDIGO risk stratification grid (1). Patient education is a continuous and critical component of care. It should focus on medication adherence, dietary restrictions (low salt, moderate protein, and potentially low potassium/phosphate in later stages), smoking cessation, and crucially, "sick day rules." Patients must be taught to temporarily stop certain medications (like ACEi/ARBs, SGLT2i, NSAIDs, Metformin) during episodes of acute illness with vomiting, diarrhea, or fever to prevent AKI. Discussions about the different modalities of renal replacement therapy (RRT) — hemodialysis, peritoneal dialysis, and transplantation — should begin early, ideally when the eGFR approaches 20-30 mL/min/m², to allow for unhurried, shared decision-making and timely preparation.

When to Escalate

Clear, low-threshold triggers must be established for when a house officer must seek senior help to ensure patient safety.

Call Your Senior (MO/Specialist) if:

  • The patient develops any acute uremic symptoms (e.g., pericarditic chest pain, confusion, intractable vomiting, asterixis).

  • There is severe, refractory hyperkalemia (>6.0 mmol/L despite initial treatment) or severe metabolic acidosis (Bicarbonate <15 mmol/L).

  • There is an unexplained, acute drop in GFR of >25% from baseline.

  • The patient has a new diagnosis of a nephritic or nephrotic syndrome, or active urine sediment with RBC casts, suggesting an aggressive glomerulonephritis.

  • The patient has severe, uncontrolled hypertension despite multiple oral agents.

Referral Criteria:

  • Refer to the Nephrology team for all patients with a GFR <30 mL/min/1.73 m² (Stage G4/G5) for co-management and RRT planning.

  • Refer any patient with a rapid rate of progression (e.g., >5 mL/min/1.73 m² GFR loss in one year).

  • Refer if the underlying cause of CKD remains uncertain after initial workup.

  • Refer all suitable patients to a registered dietitian for medical nutrition therapy.

  • Refer to a vascular surgeon for the timely creation of a permanent dialysis access (fistula or graft) well in advance of anticipated dialysis initiation.

References

  1. Ministry of Health Malaysia. (2018). Clinical Practice Guidelines: Management of Chronic Kidney Disease (Second Edition). Putrajaya: MOH. https://www.moh.gov.my/moh/resources/penerbitan/CPG/CPG%20Management%20of%20Chronic%20Kidney%20%20Disease%20(Second%20Edition).pdf

  2. Ministry of Health Malaysia. (2018). Quick Reference for Healthcare Providers: Management of Chronic Kidney Disease (Second Edition). https://www.moh.gov.my/moh/resources/penerbitan/CPG/QR%20Management%20of%20Chronic%20Kidney%20%20Disease%20(Second%20Edition).pdf

  3. Dr.Oracle AI. (2025). What are the clinical practice guidelines (CPG) for managing Chronic Kidney Disease (CKD) and Acute Kidney Injury (AKI) in Malaysia? https://www.droracle.ai/articles/165325/cpg-ckd-aki-malaysia-sunmarised

  4. Levin, A., et al. (2024). Executive summary of the KDIGO 2024 Clinical Practice Guideline for the Evaluation and Management of Chronic Kidney Disease. Kidney International. https://kdigo.org/wp-content/uploads/2017/02/KDIGO-2024-CKD-Guideline-Executive-Summary.pdf

  5. Kalantar-Zadeh, K., & Fouque, D. (2017). Nutritional Management of Chronic Kidney Disease. New England Journal of Medicine, 377(18), 1765–1776.

  6. Jager, K. J., et al. (2019). A single number for advocacy and communication—worldwide more than 850 million individuals have kidney diseases. Kidney International, 96(5), 1048-1050.

  7. Kidney Disease: Improving Global Outcomes (KDIGO) CKD Work Group. (2013). KDIGO 2012 Clinical Practice Guideline for the Evaluation and Management of Chronic Kidney Disease. Kidney International Supplements, 3(1), 1–150. https://pmc.ncbi.nlm.nih.gov/articles/PMC4089693/

  8. Edemekong, P. F., & Bomback, A. S. (2023). Nephritic Syndrome. In StatPearls. StatPearls Publishing. https://www.ncbi.nlm.nih.gov/books/NBK562240/

  9. Kidney Disease: Improving Global Outcomes (KDIGO). (2024). KDIGO 2024 Clinical Practice Guideline for the Evaluation and Management of Chronic Kidney Disease. https://kdigo.org/wp-content/uploads/2024/03/KDIGO-2024-CKD-Guideline.pdf

  10. A.D.A.M. Medical Encyclopedia. (2023). Chronic kidney disease. https://e-mfp.org/wp-content/uploads/R1RVA-practical-approach.pdf

  11. Kidney Disease: Improving Global Outcomes (KDIGO). (2024). Top 10 Takeaways on Evaluation for Primary Care Physicians from the KDIGO 2024 Guideline. https://kdigo.org/wp-content/uploads/2024/03/KDIGO-2024-CKD-Guideline-Top-10-Takeaways-for-PCPs-Evaluation.pdf

  12. Cleveland Clinic. (2022). Chronic Kidney Disease (CKD): Symptoms & Treatment. https://my.clevelandclinic.org/health/diseases/15096-chronic-kidney-disease

  13. Hooi, L. S., et al. (2020). Prevalence of chronic kidney disease and its associated factors in Malaysia; findings from a nationwide population-based cross-sectional study. PLoS ONE, 15(8), e0237862. https://pubmed.ncbi.nlm.nih.gov/32795256/

  14. Jankowski, J., et al. (2021). Cardiovascular Disease in Chronic Kidney Disease. Circulation, 143(11), 1157–1172. https://www.ahajournals.org/doi/10.1161/CIRCULATIONAHA.120.050686

  15. Ministry of Health Malaysia. (2022). National Strategic Plan for Kidney Disease (ACT-KID). https://www.moh.gov.my/moh/resources/Penerbitan/Rujukan/NCD/National%20Strategic%20Plan/act_kid-1-min.pdf

  16. Remuzzi, G., & Bertani, T. (1998). Pathophysiology of progressive nephropathies. New England Journal of Medicine, 339(20), 1448-1456.

  17. Nath, K. A. (1998). Tubulointerstitial changes as a major determinant in the progression of real disease. American Journal of Kidney Diseases, 32(4), 697-700.

  18. Lau, W. L., & Vaziri, N. D. (2017). Uremia. In StatPearls. StatPearls Publishing. https://www.ncbi.nlm.nih.gov/books/NBK441859/

  19. Cleveland Clinic. (2021). Uremia: Causes, Symptoms, Diagnosis & Treatment. https://my.clevelandclinic.org/health/diseases/21509-uremia

  20. Wanner, C., et al. (2016). Cardiovascular disease in chronic kidney disease: Pathophysiological insights and therapeutic options. European Heart Journal, 37(38), 2917–2926.

  21. Liyanage, T., et al. (2022). The Etiology of Advanced Chronic Kidney Disease in Southeast Asia: A Meta-analysis. Kidney International Reports, 7(6), 1249-1260. https://pmc.ncbi.nlm.nih.gov/articles/PMC11442843/

  22. American Diabetes Association. (2023). Standards of Medical Care in Diabetes—2023. Diabetes Care, 46(Supplement_1).

  23. The Malaysian Reserve. (2024). Malaysia on brink of kidney disease crisis. https://themalaysianreserve.com/2024/03/14/malaysia-on-brink-of-kidney-disease-crisis/

  24. Centers for Disease Control and Prevention. (2023). Chronic Kidney Disease Basics. https://www.cdc.gov/kidney-disease/about/index.html

  25. Hooi, L.S., et al. (2018). Burden of chronic kidney disease and its risk factors in Malaysia. BMC Public Health, 18(1), 1-9.

  26. National Kidney Foundation. (2022). 10 Signs You May Have Kidney Disease. https://www.kidney.org/news-stories/10-signs-you-may-have-kidney-disease

  27. National Health Service. (2021). Chronic kidney disease - Symptoms. https://www.nhs.uk/conditions/kidney-disease/symptoms/

  28. Merck Manual Professional Version. (2023). Chronic Kidney Disease. https://www.merckmanuals.com/professional/genitourinary-disorders/chronic-kidney-disease/chronic-kidney-disease

  29. Mayo Clinic. (2023). End-stage renal disease - Symptoms and causes. https://www.mayoclinic.org/diseases-conditions/end-stage-renal-disease/symptoms-causes/syc-20354532

  30. Lim, Y. N., et al. (2014). Chronic Kidney Disease Screening Methods and Its Implication for Malaysia: An in Depth Review. BioMed Research International, 2014, 903495. https://pmc.ncbi.nlm.nih.gov/articles/PMC4802081/

  31. Kidney Disease: Improving Global Outcomes (KDIGO). (2024). Evaluation and Management of Chronic Kidney Disease: Synopsis of the KDIGO 2024 Clinical Practice Guideline. Annals of Internal Medicine. https://www.acpjournals.org/doi/10.7326/ANNALS-24-01926

  32. Kidney Disease: Improving Global Outcomes (KDIGO). (2024). KDIGO 2025 Clinical Practice Guideline for Anemia in Chronic Kidney Disease (Public Review Draft). https://kdigo.org/wp-content/uploads/2024/11/KDIGO-2025-Anemia-in-CKD-Guideline_Public-Review-Draft_Nov42024.pdf

  33. Malaysian Society of Nephrology. (2018). 1st Malaysian CKD MBD and Parathyroidectomy Guidelines. https://www.researchgate.net/publication/328730162_1st_Malaysian_CKD_MBD_and_Parathyroidectomy_Guidelines_SOP

  34. Wesson, D. E., & Simoni, J. (2019). Treatment of Metabolic Acidosis in Patients With CKD. American Journal of Kidney Diseases, 74(3), 376-383. https://pmc.ncbi.nlm.nih.gov/articles/PMC3946919/

Danial Mirza
Next

Acute Kidney Injury: A Clinical Guide