CHRONIC KIDNEY DISEASE Flashcards
What is the prevalence of treated kidney failure in the Philippines?
319 per million people, with 314 receiving chronic dialysis.
Which type of dialysis is more common in the Philippines, hemodialysis or peritoneal dialysis?
Hemodialysis.
What does Figure 2 represent?
CKD and its risk factors burden.
What does Figure 3 show about Southeast Asia?
Southeast Asia has a significantly higher chronic kidney disease disability-adjusted life-year (DALY) rate compared to other regions.
What is Conservative Kidney Management (CKM)?
CKM refers to managing patients with medications and lifestyle changes instead of renal replacement therapy, despite being candidates for it.
What is the ratio of nephrologists to the population in the Philippines?
8.87 nephrologists per million population.
How many nephrologists are in the Philippines according to the Philippine Society of Nephrology?
888 nephrologists.
What is the initial step in managing CKD, similar to acute kidney injury?
Identify individuals at risk, followed by testing, stratification, treatment, monitoring, and referral.
What is the time frame for diagnosing CKD?
Kidney damage or reduced GFR present for a minimum of 3 months.
What are the stages of chronic kidney disease based on GFR?
G1 to G5, with G1 being the best and G5 the most severe.
What are the albuminuria categories in CKD?
A1 to A3, where A1 is normal to mildly increased, A2 is moderately increased, and A3 is severely increased.
What are markers of kidney damage that can indicate CKD?
Albuminuria (ACR ≥30 mg/g), urine sediment abnormalities, persistent hematuria, electrolyte abnormalities, structural abnormalities, histology findings, or history of kidney transplantation.
What GFR level is considered decreased and indicative of CKD?
GFR <60 ml/min per 1.73 m² (categories G3a-G5).
How does KDIGO define CKD?
Abnormalities of kidney structure or function present for a minimum of 3 months with implications for health.
What does the CGA classification of CKD stand for?
Cause, GFR category (G1-G5), and Albuminuria category (A1-A3).
What is the first-line therapy for CKD patients according to KDIGO?
Lifestyle changes and SGLT2 inhibitors, along with ACE inhibitors or ARBs and statins.
What is the conversion factor for albumin-to-creatinine ratio (ACR) from mg/g to mg/mmol?
0.113.
What is the conversion factor for calcium from mg/dl to mg/mmol?
0.2495.
What is the conversion factor for creatinine from mg/dl to µmol/l?
88.4.
What is the conversion factor for phosphate from mg/dl to mmol/l?
0.3229.
What are the approximate equivalent albuminuria categories in CKD?
A1: <30 mg/g, A2: 30-300 mg/g, A3: >300 mg/g.
What is the focus of Figure 11 regarding CKD care?
Special considerations for chronic kidney disease care across the lifespan.
What does CKD encompass?
A spectrum of pathophysiologic processes associated with abnormal kidney function and progressive decline in glomerular filtration rate.
What are the two parameters of CKD?
Abnormal kidney disease and progressive GFR decline.
What are the basic physiologic mechanisms of the nephron?
Filtration, secretion, reabsorption, and excretion.
What is the risk of CKD progression closely linked to?
Both the GFR and the amount of albuminuria.
What is end-stage renal disease?
A stage of CKD where toxins, fluid, and electrolytes accumulate, leading to death unless treated with renal replacement therapy.
What are the two sets of mechanisms in CKD pathophysiology?
Initiating mechanisms and hyperfiltration mechanisms.
What are initiating mechanisms in CKD?
Specific conditions causing CKD, such as toxin exposure or deposition of immune complexes (e.g., glomerulonephritides).
What is hyperfiltration in CKD?
A compensatory mechanism where remaining viable nephrons hyperfilter and hypertrophy to maintain GFR temporarily.
What happens in a hyperfiltering glomerulus?
Damaged endothelium, sclerosis, and enlarged arterioles lead to long-term glomerular damage despite temporary GFR maintenance.
What are non-modifiable risk factors for CKD?
Small for gestational age, advanced age, African ancestry, family history of kidney disease, and previous AKI.
What are modifiable risk factors for CKD?
Childhood obesity, hypertension, diabetes, proteinuria, and lifestyle factors such as smoking and diet.
What are risk factors for CKD progression in adulthood?
Elevated blood pressure, treated childhood kidney disease, and nephrotoxic exposures.
What is the effect of healthy aging on GFR?
GFR declines by 1 ml/min per year starting from the 3rd decade of life.
What structural changes occur in kidneys with aging?
Global glomerulosclerosis, interstitial fibrosis, and arteriosclerosis.
What is GFR?
The amount of fluid filtered into the Bowman space per unit of time, dependent on glomerular membrane porosity, surface area, and pressure.
What is the normal GFR value?
Greater than 90 mL/min/1.73 m².
What is eGFR, and why is it used?
Estimated GFR calculated using plasma creatinine; it is used for CKD detection, monitoring, and prognostication.
What are the common eGFR calculation methods?
Cockcroft-Gault (CG), MDRD, and CKD-EPI equations.
What is proteinuria, and why is it important in CKD?
One of the earliest markers of renal disease, providing diagnostic and prognostic information for CKD.
What are casts in urine, and what do they indicate?
Cylindrical bodies of renal origin; red cell casts indicate significant glomerular pathology.
How is creatinine clearance (CrCl) measured?
By collecting 24-hour urine and measuring total excreted creatinine and urine volume.
What is the Cockcroft-Gault formula for CrCl?
CrCl = [(140-age) x lean body weight (kg)] / [Serum Creatinine (mg/dL) x 72] (x 0.85 if female).
What is the CKD-EPI formula for eGFR?
eGFR = 141 x min(PCr/k, 1)^a x max(PCr/k, 1)^-1.209 x 0.993^age x 1.018 [if female] x 1.159 [if black].
What are the modifiable interventions to slow CKD progression?
Hypertension control, glycemic control, proteinuria management, and lifestyle changes such as smoking cessation.
What medications are recommended for CKD management?
SGLT-2 inhibitors, ACE inhibitors or ARBs, diuretics, and sodium bicarbonate for metabolic acidosis.
What are the non-modifiable demographic risk factors for CKD?
Old age, male sex, Hispanic or African-American ancestry, and low birth weight.
What are nephrotoxic exposures contributing to CKD?
Heavy metals, environmental toxins, and certain antineoplastic therapies.
What is the main utility of eGFR equations?
Detection, monitoring, and prognostication of CKD.
What is the limitation of creatinine as a marker for renal function?
It is insensitive to significant declines in GFR at the upper limit of normal due to compensatory hyperfiltration.
What is the clinical significance of proteinuria in CKD?
It occurs before a reduction in GFR and aids in diagnosis and stratification of CKD severity.
What is the eGFR range for Stage 1 CKD, and what are its clinical features?
eGFR >60 mL/min/1.73 m²; Abnormal urinalysis and renal imaging.
What is the importance of identifying Stage 1 CKD?
Risk of progression to later stages increases with proteinuria and depends on the cause of the disease.
What is the eGFR range for Stage 2 CKD, and what are its clinical features?
eGFR >60 mL/min/1.73 m²; Abnormal urinalysis and renal imaging.
What is the risk associated with Stage 2 CKD?
Mild risk of progression, which increases with proteinuria and depends on the cause of the disease.
What is the eGFR range for Stage 3a CKD, and what are its clinical features?
eGFR 45–60 mL/min/1.73 m²; Cardiovascular disease or other organ damage.
What is the focus for Stage 3a CKD management?
Moderate risk of progression; focus on vascular risk factors like high BP, lipids, smoking, and weight.
What is the eGFR range for Stage 3b CKD, and what are its clinical features?
eGFR 30–45 mL/min/1.73 m²; Proteinuria.
What is the risk associated with Stage 3b CKD?
High risk of disease progression.
What is the eGFR range for Stage 4 CKD, and what are its clinical features?
eGFR 15–30 mL/min/1.73 m²; High likelihood of progression to ESRD.
What preparations are needed for Stage 4 CKD?
Prepare and educate regarding renal replacement therapy options, including dialysis and transplant.
What is the eGFR range for Stage 5 CKD, and what are its clinical features?
eGFR <15 mL/min/1.73 m²; Highest risk of requiring renal replacement therapy.
What does KDIGO use to classify CKD prognosis?
GFR categories (G1–G5) and albuminuria levels (A1–A3).
What is the significance of albuminuria in CKD?
A prognostic indicator for microvascular disease and endothelial dysfunction.
What does green signify in the KDIGO risk chart?
Low risk for CKD progression.
What does red signify in the KDIGO risk chart?
High risk for CKD progression.
What are the signs and symptoms of CKD affecting the body?
CKD affects every organ system, progressing to uremic syndrome in advanced stages.
What happens to GFR in healthy aging?
GFR declines by 1 mL/min per year starting in the 3rd decade of life.
What happens in Uremic Syndrome?
A constellation of signs and symptoms pointing to kidney failure, with toxins affecting other organ systems.
What are the metabolic effects of uremia?
Increased oxidant levels, reduced energy expenditure, insulin resistance, muscle wasting, and sexual dysfunction.
What neural and muscular symptoms are seen in uremia?
Fatigue, sleep disturbances, restless legs, peripheral neuropathy, and reduced muscle membrane potential.
What other symptoms can occur with uremia?
Serositis, hiccups, platelet dysfunction, shortened erythrocyte lifespan, and granulocyte dysfunction.
What are common etiologies of CKD?
Diabetic nephropathy, glomerulonephritis, hypertension-associated CKD, and polycystic kidney disease.
What are the renoprotective effects of ACE inhibitors?
Lower systemic BP, lower glomerular pressure, increased renal blood flow, reduced proteinuria, and natriuretic effects.
What cardiovascular benefits do ACE inhibitors provide?
Inhibition of LV remodeling and reduction in cardiac workload.
What is the significance of BUN and creatinine in CKD?
They measure kidney excretory function but don’t account for all symptoms of uremia.
What are some uremic toxins aside from BUN and creatinine?
Middle molecules and other toxins not routinely measured contribute to CKD symptoms.
What is the role of albumin oxidation in CKD?
Contributes to systemic inflammation and progression of kidney damage.
What is the pathogenesis of progressive renal injury in CKD?
Nephron loss leads to chronic inflammation, glomerulosclerosis, and tubulointerstitial fibrosis.
Why is angiotensin II important in CKD pathophysiology?
Angiotensin II promotes glomerulosclerosis and fibrosis through hemodynamic and non-hemodynamic effects.
What are the systemic effects of CKD on the cardiovascular system?
Hypertension, LV hypertrophy, vascular calcification, and accelerated atherosclerosis.
What is the primary cause of hypertension and peripheral edema in CKD?
Sodium and water retention due to decreased sodium excretion.
What dietary advice is given to CKD patients to manage water and sodium balance?
Patients should restrict salt and water intake.
Why is blood pressure difficult to control in CKD patients, even on dialysis?
CKD disrupts sodium balance, leading to hypertension that often requires multiple medications.
What happens to sodium and water excretion in CKD patients with fluid loss (e.g., diarrhea)?
The kidneys fail to conserve sodium and water, leading to volume depletion.
What is the treatment for sodium and water retention in CKD?
Diuretics and water restriction.
What causes hyperkalemia in CKD?
Progressive decline in GFR reduces potassium excretion, leading to serum potassium accumulation.
What is the role of the renin-angiotensin-aldosterone system (RAAS) in potassium balance?
RAAS activation increases aldosterone, promoting potassium excretion in the distal tubules and collecting ducts.
What treatments are available for chronic hyperkalemia?
Potassium-binding resins like Patiromer and Sodium Zirconium Cyclosilicate.
What causes metabolic acidosis in CKD?
Failure of the kidneys to acidify urine, leading to retention of excess acids.
What are the consequences of persistent metabolic acidosis in CKD?
Increased protein catabolism, muscle wasting, and cachexia.
How does hyperkalemia aggravate metabolic acidosis in CKD?
Hyperkalemia suppresses ammonia formation, reducing acid excretion.
What is the treatment for metabolic acidosis in CKD?
Sodium bicarbonate supplementation to reduce protein catabolism and correct acidosis.
What are the main bone-related complications in CKD?
Mineral bone disease and renal osteodystrophy.
What defines CKD-Mineral Bone Disease (CKD-MBD)?
A systemic disorder of mineral and bone metabolism due to CKD, manifesting as abnormalities in calcium, phosphorus, PTH, or vitamin D metabolism, bone turnover, or vascular calcification.
What is the hallmark lesion of secondary hyperparathyroidism in CKD?
Osteitis fibrosa cystica.
What causes osteomalacia in CKD?
Reduced bone mineralization due to vitamin D deficiency.
What is calciphylaxis, and why is it fatal?
Calciphylaxis is caused by calcium deposition in the vascular system, leading to ischemic necrosis and organ damage.
What is the significance of vascular calcification in CKD?
It contributes to vascular occlusion, cardiovascular disease, and increased mortality.
What is tumoral calcinosis in CKD?
Painful calcium deposits in soft tissues, often due to chronic hyperphosphatemia.
What is the leading cause of death in CKD patients?
Cardiovascular disease (CVD).
How does CKD increase the risk of CVD?
CKD causes inflammation, vascular calcification, and sympathetic overactivity, leading to complications like LVH and heart failure.
What is uremic pericarditis?
Inflammation of the pericardium in advanced CKD, often requiring dialysis as treatment.
What is the target blood pressure for CKD patients with diabetes or proteinuria?
<130/80 mmHg.
Why are ACE inhibitors and ARBs preferred for CKD management?
They slow the progression of kidney disease and reduce proteinuria.
What causes anemia in CKD?
Relative erythropoietin deficiency, iron deficiency, and chronic inflammation.
What is the treatment for anemia in CKD?
Erythropoiesis-stimulating agents (ESAs) and iron supplementation.
What is the role of erythropoiesis-stimulating agents (ESAs) in CKD?
ESAs stimulate red blood cell production to reduce the need for blood transfusions.
What is the ideal target hemoglobin level in CKD patients on ESA therapy?
102–110 g/L.
What is the bat-wing appearance in CKD-related pulmonary edema?
Alveolar fluid accumulation seen in imaging, caused by increased permeability of pulmonary capillaries.
Why is hypertension common in CKD patients?
Early disruption of sodium and water balance leads to increased blood pressure and LV hypertrophy.
How does CKD exacerbate heart failure?
Anemia and hypertension increase the workload on the heart, leading to cardiac complications.
What is the impact of RAAS activation in CKD?
It leads to vascular constriction, increased BP, and progression of kidney damage.
Why are CKD patients at higher risk of sudden cardiac death?
Electrolyte imbalances, LV hypertrophy, and intradialytic hypotension contribute to arrhythmias.
What are the common hematologic complications in CKD?
Abnormal bleeding time (diathesis) and coagulopathy, often manifested as excessive bleeding.
What are the neurologic complications of CKD?
CNS issues (confusion, sleep disturbances, seizures), neuromuscular problems (cramps, hiccups, muscle twitching), and peripheral neuropathy.
What is the efficiency of dialysis compared to normal kidney function?
Dialysis functions at approximately 5% of the capacity of a normal kidney.
What are the GI complications in CKD?
Abdominal pain, mucosal ulceration, GI bleeding, constipation, nausea, vomiting, and weight loss.
Why might insulin doses need adjustment in CKD?
Decreased clearance of insulin leads to higher insulin levels in the blood.
What are the endocrine effects of CKD in women?
Low estrogen levels, menstrual abnormalities, infertility, and difficulties in pregnancy.
What are the endocrine effects of CKD in men?
Low testosterone levels and sexual dysfunction, though some dialysis patients may exhibit a high libido.
What is nephrogenic systemic fibrosis?
A systemic induration of subcutaneous tissue, usually after gadolinium contrast exposure in patients with GFR <30.
What causes dark skin pigmentation in CKD patients?
Deposition of urochromes due to retained pigment metabolites, even in dialysis.
What are the key lab investigations for CKD?
CBC, creatinine, BUN, electrolytes, ABG, urinalysis, and specific tests like serum electrophoresis or kidney biopsy.
What is renal scintigraphy used for?
To assess kidney function, anatomy, and pathology using radioactive tracers like Tc-99m DTPA or Tc-99m DMSA.
What is the most useful imaging test for kidneys?
Renal ultrasound.
What are the exceptions where CKD may not cause shrunken kidneys?
Diabetes, amyloidosis, HIV, and APKD (autosomal polycystic kidney disease).
What does the KDIGO classification system provide for CKD?
Risk stratification and a framework for guiding management through CKD stages.
What lifestyle changes are recommended for CKD patients?
Smoking cessation, weight loss, and dietary sodium restriction.
What is the first-line antihypertensive therapy for CKD with albuminuria?
ACE inhibitors or angiotensin receptor blockers (ARBs).
What are the dietary recommendations for CKD patients?
Low sodium (<5g/day), potassium restriction (if CKD stage 3-5), and phosphorus reduction.
What is the recommended protein intake for CKD patients?
0.8g/kg/day.
What is calciphylaxis, and why is it dangerous in CKD?
Calcium buildup in the vascular system leading to ischemic necrosis and high fatality.
What is the significance of hyperkalemia in CKD?
It results from reduced potassium excretion due to declining GFR, leading to fatal complications if untreated.
What treatments are available for chronic hyperkalemia?
Potassium-binding resins like Patiromer or Sodium Zirconium Cyclosilicate.
What causes metabolic acidosis in CKD?
Failure of the kidneys to excrete excess acids, leading to retention of protons.
What is the treatment for metabolic acidosis in CKD?
Sodium bicarbonate supplementation.
What are the bone complications of CKD?
Mineral bone disease, renal osteodystrophy, and vascular calcifications.
What is the hallmark lesion of secondary hyperparathyroidism in CKD?
Osteitis fibrosa cystica.
What is renal replacement therapy (RRT)?
Therapies like hemodialysis, peritoneal dialysis, and kidney transplantation to replace kidney function.
What is Conservative Kidney Management (CKM)?
Symptomatic treatment for CKD patients who decline or cannot afford RRT.
What are the dietary restrictions for CKD patients?
Low sodium, phosphorus, and potassium (if CKD stage 3-5); emphasis on plant-based proteins and whole foods.
What is the effect of intraglomerular hypertension in CKD?
It leads to maladaptive changes, accelerating kidney damage.
Which medications need dose adjustments in CKD?
Drugs excreted or metabolized by kidneys, e.g., antibiotics (penicillin, cephalosporins) and metformin.
What is the role of ACE inhibitors/ARBs in CKD management?
They slow CKD progression by reducing intraglomerular hypertension and proteinuria.
What is the target BP for CKD patients with diabetes or proteinuria?
<130/80 mmHg.
What are the indications to start dialysis in CKD?
Symptoms like uremic syndrome, volume overload, or persistent electrolyte abnormalities.
What is uremic pericarditis?
A complication of advanced CKD, characterized by chest pain and pericardial friction rub.
What is the most common cause of death in CKD patients?
Cardiovascular disease.
What is the bat-wing appearance in pulmonary edema related to CKD?
Alveolar fluid accumulation seen in imaging, caused by capillary permeability changes.
What are the risk factors for CKD progression?
Hypertension, proteinuria, poor glycemic control, and lifestyle factors like smoking.
What is the importance of serial creatinine monitoring in CKD?
It helps detect progression or sudden changes in kidney function.
What is the clinical benefit of starting renal replacement therapy (RRT) early in asymptomatic CKD patients?
There is no clinical or mortality benefit compared to starting RRT when symptoms of uremia appear.
What is the most ideal form of renal replacement therapy (RRT) for CKD patients?
Kidney transplantation (KT) as it replaces all kidney functions, unlike dialysis which only manages excretory functions.
What is preemptive dialysis?
Dialysis initiated before symptoms appear; it does not guarantee survival benefits over starting dialysis with clear indications.
When should CKD patients be educated about RRT?
Before reaching CKD stage 5 and the onset of uremic symptoms.
What dietary restrictions are suggested for CKD patients with fluid overload?
Salt <2.4 g/day; water intake depends on urine volume.
What dietary adjustments are suggested for CKD patients with hyperkalemia?
Avoid high potassium intake, stop RAAS inhibitors, correct acidosis, and use potassium exchangers.
What is the target calcium and phosphate balance in CKD patients?
Calcium × phosphate product <55 mg²/mL², phosphate <4.5 mg/dL, and total elemental calcium <2,000 mg/day.
What are the monitoring intervals for calcium and phosphate levels in CKD?
CKD 3: every 6-12 months; CKD 4: every 3-6 months; CKD 5: every 1-3 months.
What is the treatment for hyperparathyroidism in CKD?
Correct hyperphosphatemia and hypocalcemia, and use calcimimetics, calcitriol, or vitamin D analogs.
What are the hemoglobin monitoring intervals for CKD patients?
CKD 3: annually; CKD 4-5ND: every 6 months; CKD 5D: every 3 months.
What is the iron treatment threshold for CKD patients?
TSAT <30% and ferritin <500 ng/mL warrant iron therapy.
What is the recommended protein intake for non-dialysis CKD patients?
0.7–0.8 g/kg of ideal body weight/day.
What is the recommended protein intake for dialysis patients?
1.2 g/kg of ideal body weight/day.
What is the dietary potassium recommendation for CKD stage 3 and 4 patients?
2–4 g/day, adjusted as tolerated.
What are the dietary phosphorus restrictions for CKD patients?
<800 mg/day, with an emphasis on plant-based sources over animal-based sources.
What is the target blood pressure for CKD patients with proteinuria?
<130/80 mmHg.
What is the target hemoglobin level for CKD patients on ESA therapy?
10–11.5 g/dL; stop ESA if hemoglobin exceeds 13 g/dL.
What lifestyle recommendations are important for CKD patients?
Smoking cessation, moderate exercise (30–60 min/day, 4–7 days/week), and a DASH diet with <5 g/day salt.
What are the dietary strategies to minimize CKD progression?
Reduce dietary acid load, emphasize plant-based foods, and minimize red meat and processed food intake.
What is the role of SGLT2 inhibitors in CKD management?
They provide renal and cardiovascular protection, even in non-diabetic patients.
What are the complications of hyperkalemia in CKD?
Hyperkalemia can lead to fatal arrhythmias if not managed effectively.
What is the importance of dietary fiber in CKD?
≥25 g/day of fiber helps maintain a healthy gut microbiome and reduces uremic toxin production.
What are the goals for anemia management in CKD?
Maintain hemoglobin levels between 10–11.5 g/dL, treat with ESA and iron, and avoid red cell transfusions unless urgent.
What is the significance of dietary sodium restriction in CKD?
It helps control blood pressure, reduces fluid retention, and slows CKD progression.
What are signs of irreversible kidney damage in CKD?
Glomerulosclerosis, fibrosis, and tubular injury.
What is the role of plant-based diets in CKD?
They reduce CKD progression, minimize uremic symptoms, and improve overall mortality risk.
What are the main mechanisms driving CKD progression?
Glomerular capillary hypertension, proteinuria, tubulointerstitial fibrosis, oxidative stress, and acidosis.
What are the therapeutic goals for renoprotection in CKD?
Reduce glomerular capillary pressure, manage metabolic acidosis, and use RAAS or SGLT2 inhibitors.
When is renal scintigraphy indicated in CKD?
To assess kidney function, anatomy, or earlier kidney injuries using radioactive tracers.
What are the key findings in nephron loss in CKD?
Progressive nephron loss leads to maladaptive glomerular hypertrophy and hypertension, further accelerating damage.
What is the importance of early preparation for RRT in CKD stage 4?
Educating patients about RRT options helps them make informed decisions before reaching end-stage renal disease.
What is the dietary protein recommendation to delay CKD progression?
0.7–0.8 g/kg/day for non-dialysis patients and incorporating plant-based protein sources.
What are common dietary interventions to manage CKD-related complications?
Low sodium, potassium restriction (if indicated), phosphorus limitation, and plant-based diets.
What is the primary dietary recommendation for CKD patients with mineral and bone disorders?
Restrict phosphate intake to <800–1,000 mg/day and maintain calcium-phosphate balance.
What is the role of probiotics in CKD management?
Probiotics help correct gut dysbiosis, promoting kidney health by reducing uremic toxin production.
What are the indications for referral to a nephrologist in CKD?
Proteinuria >0.5 g/day, rapid GFR decline, and advanced CKD (stage 4-5).
What is the impact of metabolic acidosis in CKD?
It accelerates protein catabolism, muscle wasting, and CKD progression.
What dietary approach minimizes net endogenous acid production in CKD?
Promote plant-based, base-producing fruits and vegetables while minimizing animal-based protein.
What is the goal of CKD management with RAAS inhibitors?
Reduce proteinuria, intraglomerular pressure, and slow CKD progression.
What is the typical course of GFR and UAE in diabetic kidney disease (DKD)?
GFR may peak in prediabetes or shortly after diabetes diagnosis, and UAE remains normal during the silent period, but GFR loss accelerates with macroalbuminuria.
What is whole-kidney hyperfiltration in DKD?
A GFR exceeding approximately 135 mL/min.
Why is albuminuria not a sensitive marker for early DKD?
Albuminuria remains normal during the silent period, while DKD lesions progress subclinically.
What is the role of kidney biopsy in DKD?
Provides insights into the severity and prognosis of DKD but has limited predictive value for early progression to ESKD.
What are biomarkers available in the Philippines for tubular damage?
Cystatin C and NGAL.
What does ‘glucose memory’ refer to in DKD?
Persistent epigenetic changes causing diabetic complications even after normalization of hyperglycemia.
What is the main focus of new treatment strategies for DKD?
Targeting beyond glycemia, including pathways involving epigenetics, inflammation, and fibrosis.
What factors contribute to glomerular hyperfiltration in diabetes?
Reduced afferent arteriolar resistance, increased efferent resistance, and hormonal influences like glucagon and vasopressin.
What is the effect of intensive glucose control on kidney outcomes?
Reduces ESKD risk but compliance is challenging, especially in older or acutely ill patients.
What are the classes of diabetic kidney disease based on glomerular lesions?
Class I: Mild/nonspecific changes; Class IIa: Mild mesangial expansion; Class IIb: Severe mesangial expansion; Class III: Nodular sclerosis; Class IV: Advanced diabetic glomerulosclerosis.
What is the significance of mesangial expansion in DKD?
Severe mesangial expansion is associated with advanced DKD and progressive GFR decline.
What is the effect of SGLT2 inhibitors in DKD?
Improves GFR and provides renal and cardiovascular protection even in non-diabetic patients.
What are potential limitations of metformin in DKD?
Requires dose modification or discontinuation at low eGFR (<30 mL/min) due to increased risk of lactic acidosis.
Why are sulfonylureas risky in DKD?
They increase the risk of hypoglycemia due to active metabolite accumulation.
What are the risks of thiazolidinediones in DKD?
Cause fluid retention and increased risk of congestive heart failure.
What is the mechanism of action of SGLT2 inhibitors?
Promote glucose excretion through urine, reducing hyperglycemia and renal damage.
What is the relationship between CKD, diabetes, and hypoglycemia?
CKD patients with diabetes have the highest risk of severe hypoglycemia due to reduced renal insulin clearance.
What is the role of RAAS blockers in DKD management?
Reduce proteinuria, glomerular capillary pressure, and slow progression of kidney damage.
What is the dietary recommendation for protein intake in DKD?
0.7–0.8 g/kg/day for non-dialysis patients and ketoanalogue supplementation to prevent malnutrition.
What are emerging therapeutic targets in DKD?
Epigenetics, inflammation pathways, endothelin antagonists, and advanced glycation end product inhibitors.
What are key lifestyle recommendations for DKD patients?
Control blood pressure, reduce dietary sodium, exercise regularly, and avoid smoking.
What are the primary goals of DKD management?
Slow progression to ESKD, reduce cardiovascular risk, and manage complications like anemia and metabolic acidosis.
What is the significance of early transplant referral in DKD?
Preserves residual renal function and prepares patients for timely renal replacement therapy.
What are the frequent challenges in managing diabetic patients with renal failure?
Hypertension, hypervolemia, glycemic control, malnutrition, and cardiovascular comorbidities.
What are potential benefits of ketoanalogue-supplemented diets in CKD?
Ameliorate metabolic disturbances, reduce proteinuria, optimize BP control, and delay RRT initiation.
What are the benefits of SGLT2 inhibitors beyond glycemic control?
Reduce cardiovascular events, death, and progression of kidney disease.
What are the effects of hypoglycemia on DKD patients?
Increases risk of cardiovascular events and complicates glucose management.
What is the new LDL target for DKD patients?
LDL <70 mg/dL, updated from <100 mg/dL.
What drugs are currently being tested for DKD treatment?
Vitamin D receptor agonists, pentoxifylline, allopurinol, endothelin antagonists, and SGLT2 inhibitors.
What is the role of finerenone in DKD?
A mineralocorticoid receptor antagonist that enhances RAAS blocker effects without increasing potassium levels.
What is the impact of oxidative stress in DKD progression?
Leads to inflammation, fibrosis, and glomerular damage.
What are non-hemodynamic factors in DKD progression?
Proteinuria, tubulointerstitial fibrosis, acidosis, and oxidative stress.
What are the benefits of ACE inhibitors and ARBs in DKD?
They reduce glomerular hypertension and albuminuria, slowing kidney disease progression.
What is the importance of understanding CKD mechanisms?
To develop multifactorial strategies for renoprotection and block CKD progression pathways at multiple points.
