Chronic Kidney Disease (CKD) | Etiology, Pathophysiology, Clinical Features, Diagnosis, Treatment

Ninja Nerd71 minutes read

Chronic kidney disease (CKD) is a condition that affects the kidneys' ability to perform essential functions, leading to complications like electrolyte imbalances, hormone disruptions, and bone disorders. Managing CKD involves addressing underlying causes such as hypertension, diabetes, and glomerulonephritis, with treatment options ranging from medications like ACE inhibitors to renal replacement therapies like dialysis.

Insights

  • Chronic kidney disease (CKD) results from kidney damage affecting functions like waste removal, electrolyte balance, and hormone production, leading to complications like hypertension and diabetes.
  • Glomerulonephritis, caused by autoimmune diseases or infections, can damage the kidneys by depositing antibody-antigen complexes in the glomerular basement membrane, impacting kidney function.
  • CKD can manifest various complications such as electrolyte imbalances, hormone disruptions, and bone disorders, necessitating treatments like ACE inhibitors, diuretics, and dialysis to manage the condition effectively.

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Recent questions

  • What is chronic kidney disease?

    CKD is a condition where the kidneys are unable to perform their functions due to continuous injury over three months, leading to issues with waste removal, water balance, electrolyte maintenance, hormone release, and enzyme activity.

  • How does hypertension contribute to CKD?

    Hypertension thickens vessel walls, reducing oxygen delivery, causing fibrosis, and glomerulosclerosis, leading to reduced kidney function and CKD development.

  • What is the impact of diabetes on CKD?

    Diabetes, specifically diabetic nephropathy, causes CKD through non-enzymatic glycation, inflammation, arteriosclerosis, and increased GFR, affecting kidney function and leading to disease progression.

  • How does glomerulonephritis affect CKD?

    Glomerulonephritis, often linked to autoimmune diseases or infections, results in antibody-antigen complex deposits in the glomerular basement membrane, causing kidney damage and contributing to CKD development.

  • How can CKD complications be managed?

    CKD complications like electrolyte imbalances, hormone disruptions, and bone disorders can be managed by addressing underlying causes such as hypertension, diabetes, glomerulonephritis, and polycystic kidney disease, along with treatments like ACE inhibitors, diuretics, and renal replacement therapies.

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Summary

00:00

Causes and Mechanisms of Chronic Kidney Disease

  • Chronic kidney disease (CKD) is the focus of the discussion.
  • The kidneys' functions include waste removal, water balance regulation, electrolyte maintenance, acid-base balance, hormone release, and enzyme activity.
  • CKD occurs when the kidneys can't perform these functions due to continuous injury over three months.
  • Renal function decline is measured by the glomerular filtration rate (GFR), with a GFR below 90 indicating CKD.
  • Hypertension is a common cause of CKD, leading to thickening of vessel walls, reduced oxygen delivery, fibrosis, and glomerulosclerosis.
  • Diabetes, specifically diabetic nephropathy, is another prevalent cause of CKD due to non-enzymatic glycation, inflammation, arteriosclerosis, and increased GFR.
  • Glomerulonephritis, often linked to autoimmune diseases or infections, can result in antibody-antigen complexes depositing in the glomerular basement membrane, causing kidney damage.
  • Mesangial cells respond to high GFR by secreting transforming growth factor beta, leading to fibrosis and glomerulosclerosis.
  • Arteriosclerosis from hypertension or diabetes can increase back pressure, hyperfiltration, and tubular disease, reducing GFR.
  • Understanding the causes and mechanisms of CKD, such as hypertension, diabetes, and glomerulonephritis, is crucial for managing and preventing kidney disease.

15:39

"Glomerulonephritis to Chronic Kidney Disease Progression"

  • In glomerulonephritis, inflammatory reactions occur in the glomerular basement membrane, leading to damage to endothelial cells, basement membrane proteins, and podocytes.
  • Antigen-antibody complex deposits increase inflammation, attracting complement proteins and white blood cells, eventually causing destruction of the glomerular basement membrane.
  • Increased porosity of the membrane due to damage results in hyperfiltration, initially increasing glomerular filtration rate (GFR) and leakage of substances into urine.
  • Mesangial cells respond to hyperfiltration by releasing transforming growth factor beta, leading to fibrosis and glomerulosclerosis, reducing GFR over time.
  • Polycystic kidney disease causes cysts to compress renal vessels, reducing blood flow to the glomerulus and other kidney tubules, affecting oxygen supply and leading to reduced GFR.
  • Compression of renal vessels by cysts triggers the release of renin, activating the renin-angiotensin-aldosterone system, causing vasoconstriction and potentially hypertension, leading to glomerulosclerosis and reduced GFR.
  • NSAID overuse inhibits prostaglandin production, leading to vasoconstriction, reduced glomerular blood flow, and decreased GFR over time, potentially causing chronic kidney disease.
  • Acute kidney injury, if not resolved or recurring frequently, can progress to chronic kidney disease due to continuous insults to the kidneys.
  • Chronic kidney disease can lead to electrolyte abnormalities, such as hyperkalemia, hyperphosphatemia, and hypocalcemia, due to reduced filtration and tubular damage.
  • Reduced kidney function in chronic kidney disease can result in water imbalance, leading to water retention, pulmonary edema, hypertension, and peripheral edema due to increased blood volume and pressure.

30:35

Complications of Chronic Kidney Disease

  • In chronic kidney disease, damaged kidney tubules and glomerulus lead to the excretion of albumin in urine, causing albuminuria.
  • Albuminuria results in decreased albumin in the blood, leading to water loss into interstitial fluid, potentially causing volume overload states like pulmonary and peripheral edema.
  • Urea accumulation due to kidney damage can progress from azotemia to uremia, causing cytotoxic effects on neurons, leading to encephalopathy with symptoms like asterixis, seizures, and coma.
  • Uremia can also cause uremic pericarditis, leading to pericardial effusions, and uremic frost on the skin due to urea crystallization.
  • Platelet dysfunction from urea accumulation increases the risk of bleeding, known as coagulopathy.
  • Chronic kidney disease affects hormone production, leading to anemia due to decreased erythropoietin and secondary hypertension from increased renin production.
  • Decreased alpha one hydroxylase enzyme in damaged kidneys results in reduced active vitamin D production, leading to decreased calcium absorption and hyperparathyroidism.
  • Hyperparathyroidism causes bone resorption, leading to renal osteodystrophy, osteitis cystica fibrosa, and increased fracture risk.
  • Chronic kidney disease impairs acid-base balance by reducing proton secretion and bicarb reabsorption, increasing proton concentration and reducing bicarb levels in the blood.
  • Overall, chronic kidney disease results in a range of complications, including electrolyte imbalances, hormone disruptions, and bone disorders, impacting various body systems and functions.

45:41

Understanding Metabolic Acidosis and Chronic Kidney Disease

  • Metabolic acidosis occurs due to an increase in protons and a decrease in bicarb, leading to a drop in pH.
  • In metabolic acidosis, there is a reduced ability to excrete protons and reabsorb bicarb, causing bicarb to end up in the urine.
  • Kidney damage can result in the spilling of albumin into the urine, lowering albumin levels in the blood.
  • Decreased albumin prompts the liver to increase protein synthesis, including lipoproteins, leading to hyperlipidemia.
  • Chronic kidney disease (CKD) diagnosis requires three months of evidence of kidney injury, often assessed through glomerular filtration rate (GFR).
  • GFR estimation can be based on creatinine or cystatin C levels, with different stages of CKD determined by GFR levels.
  • Albuminuria, the presence of albumin in urine, indicates severe kidney disease, with different levels categorized as mild, moderate, or severe.
  • Renal ultrasound can help identify causes of CKD, such as polycystic kidney disease, small atrophic kidneys, and decreased vascularity.
  • Glomerulonephritis diagnosis may require a renal biopsy to determine underlying causes, including autoimmune conditions like lupus or vasculitis.
  • Additional tests for CKD complications include monitoring potassium, phosphate, calcium, sodium, and red blood cell levels to assess disease severity.

01:00:17

Managing CKD: Tests, Treatments, and Complications

  • A BMP lab test provides information on sodium, calcium, potassium, and phosphate levels, as well as estimates GFR based on creatinine.
  • Anemia in CKD patients may be normocytic, requiring exclusion of iron deficiency anemia through iron studies.
  • Metabolic acidosis can be detected through an ABG test if BMP shows low bicarbonate levels.
  • Lipid panel tests can reveal elevated triglycerides and LDL levels in CKD patients.
  • Severe CKD can lead to increased PTH levels, potentially causing hypercalcemia, necessitating PTH level checks.
  • Treatment of CKD focuses on slowing disease progression and addressing underlying causes like hypertension, diabetes, glomerulonephritis, and polycystic kidney disease.
  • ACE inhibitors, ARBs, and diuretics are used to manage hypertension in CKD patients aiming for a BP of ≤130/80.
  • Insulin, anti-diabetic drugs, weight loss, and diet changes target high glucose levels in diabetic CKD patients.
  • Steroids and immunosuppressants like methotrexate may be used to treat glomerulonephritis, addressing autoimmune causes.
  • Discontinuing nephrotoxic agents like NSAIDs is crucial in managing CKD, while renal replacement therapies like dialysis or transplant may be needed for complications.

01:15:33

Managing Complications of Chronic Kidney Disease

  • Chronic kidney disease (CKD) complications involve electrolyte balance and secondary hyperparathyroidism.
  • Severe anemia in CKD patients may require synthetic erythropoietin if hemoglobin levels drop below 10.
  • CKD can lead to high blood pressure due to reduced glomerular filtration rate (GFR) and increased renin production.
  • Hypertension in CKD is managed with ACE inhibitors, ARBs, and potassium-sparing diuretics to inhibit the renin-angiotensin-aldosterone system.
  • Water retention in CKD can cause volume overload, managed with diuretics and sodium/water restriction.
  • Severe acidosis in CKD may require treatment with sodium bicarbonate if pH drops below 7.2.
  • Albuminuria in CKD can lead to low albumin levels, treated with ACE inhibitors or ARBs to reduce proteinuria and protect against complications like high blood pressure and increased potassium levels.
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