Ninjanerd - Chronic Kidney Disease Overview

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Questions and Answers

What is the primary characteristic of chronic kidney disease (CKD)?

An increase in Glomerular Filtration Rate (GFR) and a decrease in proteinuria

A transient increase in GFR and decreased albuminuria

Increased sodium reabsorption and decreased potassium excretion

A progressive loss of renal function, characterized by a reduction in GFR and an increase in proteinuria (correct)

What is the most common cause of chronic kidney disease?

Glomerulosclerosis due to excessive extracellular matrix secretion

Glomerulonephritis

Diabetic nephropathy (correct)

Hypertensive nephropathy

In diabetic nephropathy, what initially happens to the Glomerular Filtration Rate (GFR)?

It transiently increases due to hyperfiltration. (correct)

It remains unchanged despite increased blood pressure in the glomerulus.

It immediately decreases due to glomerular damage.

It decreases gradually due to glomerulosclerosis.

How does chronic hyperglycemia contribute to diabetic nephropathy?

By leading to non-enzymatic glycation and deposition of glycoproteins, causing efferent arteriole narrowing. (C) Signup and view all the answers

What effect does chronic high blood pressure have on the kidneys in hypertensive nephropathy?

It leads to thickening of the afferent arteriole, reducing blood flow to the glomerulus. (C) Signup and view all the answers

Which of the following best describes the pathophysiology of Glomerulonephritis?

Chronic inflammation of the glomerulus leading to increased extracellular matrix production and thickened glomerular basement membrane. (D) Signup and view all the answers

What causes metabolic acidosis in chronic kidney disease?

The kidneys' inability to filter and reabsorb bicarbonate and excrete protons. (D) Signup and view all the answers

What compensatory mechanism is used by the body to combat metabolic acidosis in CKD?

Tachypnea (Kussmaul respirations) to compensate for the acidosis by increasing respiratory drive and releasing C02. (C) Signup and view all the answers

A patient with chronic kidney disease (CKD) presents with fatigue, dyspnea, and palpitations. Which of the following is the most likely underlying cause?

Anemia of CKD (D) Signup and view all the answers

Which of the following ECG changes is most indicative of hyperkalemia?

Peaked T waves (A) Signup and view all the answers

A patient with CKD has a urine albumin to creatinine ratio of 250. This is best classified as:

Microalbuminuria (A) Signup and view all the answers

What is the preferred long-term vascular access for patients requiring hemodialysis?

AV fistula (B) Signup and view all the answers

A CKD patient's decreased GFR leads to an increase in blood pressure. What is the most direct mechanism of this effect?

Release of renin by the juxtaglomerular cells (C) Signup and view all the answers

Which of the following is a common treatment for hypervolemia in CKD patients?

Loop diuretics (B) Signup and view all the answers

What is the primary factor contributing to the development of secondary hyperparathyroidism in chronic kidney disease?

Hypocalcemia (D) Signup and view all the answers

A patient with a GFR of 25 mL/min/1.73 m2 is prescribed a new medication. What is the most important consideration related to drug dosing?

Renally dose to avoid drug toxicity (B) Signup and view all the answers

A kidney ultrasound shows bilaterally enlarged kidneys with multiple cysts. This is most suggestive of which condition?

Polycystic kidney disease (PKD) (C) Signup and view all the answers

Which of the following is a potential complication of tertiary hyperparathyroidism?

Calciphylaxis (B) Signup and view all the answers

Which of the following is a diagnostic indicator of CKD based on urinalysis?

Broad waxy casts (A) Signup and view all the answers

A patient with CKD presents with chest pain, friction rub, and diffuse ST segment elevation with PR segment depression on ECG. Which complication is most likely?

Pericarditis (A) Signup and view all the answers

Which of the following best characterizes the mechanism of secondary hypertension caused by CKD?

Increased sodium reabsorption (D) Signup and view all the answers

A patient with CKD has low serum albumin levels. Which condition might be associated due to this and is concerning?

Hyperlipidemia (C) Signup and view all the answers

A patient with CKD has a GFR of 50 mL/min/1.73 m2. Which CKD stage does this correspond to?

Stage 3A (B) Signup and view all the answers

Study Notes

Chronic Kidney Disease (CKD)

CKD is a progressive loss of renal function, characterized by a reduction in Glomerular Filtration Rate (GFR) and an increase in proteinuria, particularly albuminuria.
CKD is often caused by glomerulosclerosis, which leads to a progressive loss of nephrons and a decrease in renal function.
Glomerulosclerosis is caused by a thickening of the glomerulus and Bowman's capsule, often due to excessive extracellular matrix secretion from mesangial cells.
The most common cause of CKD is diabetic nephropathy, accounting for 40-45% of cases.
Diabetic nephropathy is caused by chronic hyperglycemia, leading to non-enzymatic glycation and deposition of glycoproteins into the efferent arteriole.
Non-enzymatic glycation narrows the efferent arteriole, increasing intra-glomerular blood pressure and inducing hyperfiltration.
Hyperfiltration is a transient increase in GFR, stimulating mesangial cells to produce more extracellular matrix, ultimately leading to glomerulosclerosis.
Diabetic nephropathy initially shows a transient increase, followed by a decrease in GFR as glomerulosclerosis advances. Albuminuria is typically an early indicator.
The second most common cause is hypertensive nephropathy, accounting for 30-35% of cases.
Hypertensive nephropathy results from chronic high blood pressure (≥140/90 mmHg), leading to afferent arteriole thickening and reduced glomerular blood flow.
The thickened afferent arteriole causes ischemia to the nephron, prompting mesangial cells to produce extracellular matrix, causing glomerulosclerosis.
Glomerulonephritis is a third common cause (10-15% of cases).
Glomerulonephritis involves chronic glomerular inflammation, stimulating mesangial cells to produce extracellular matrix and increasing the glomerular basement membrane thickness, decreasing GFR.
Patients with glomerulonephritis often exhibit significant proteinuria.

CKD Complications

Metabolic Acidosis:
- Arises from reduced GFR, impacting bicarbonate filtration/reabsorption and proton excretion.
- Elevated blood protons and decreased bicarbonate lower blood pH.
- Compensatory tachypnea (Kussmaul respirations) can occur.
- Proton/potassium exchange can lead to hyperkalemia.
- Severe acidosis causes hypotension and reduced heart contractility.
Hyperkalemia:
- Reduced GFR diminishes potassium filtration, increasing blood potassium levels.
- Characteristic ECG changes (peaked T waves, prolonged PR interval, absent P waves, widened QRS complex, sine wave) elevate risk of ventricular fibrillation.
Hypervolemia:
- Reduced GFR leads to decreased sodium/water filtration, increasing blood volume.
- Results in pulmonary edema, pleural effusions, and pitting peripheral edema.
- Can exacerbate hypertension.
Uremia:
- Elevated waste products in the bloodstream cause diverse clinical manifestations.
- Can cause altered mental status (AMS), lethargy, confusion, and coma.
- Asterixis (flapping tremor) is a potential symptom.
- Pericarditis (chest pain, friction rub, pericardial effusion, diffuse ST elevation with PR depression on ECG) is possible.
- Platelet dysfunction increases bleeding risk.
Secondary Hypertension:
- Reduced GFR stimulates juxtaglomerular (JG) cells to release renin.
- Renin converts angiotensinogen to angiotensin I, then to angiotensin II by ACE.
- Angiotensin II causes vasoconstriction, elevating blood pressure.
- Also stimulates ADH and aldosterone release, causing fluid retention and further increasing blood pressure.
Anemia of CKD:
- Reduced erythropoietin (EPO) production by peritubular cells, coupled with elevated hepcidin levels, lowers iron absorption and macrophage iron release.
- Inflammation boosts hepcidin levels.
- Fatigue, dyspnea, and palpitations are possible symptoms.
Hyperparathyroidism:
- Can be secondary or tertiary.
- Decreased GFR in CKD raises phosphate levels, reduces Vitamin D production, and triggers hypocalcemia
- Secondary: Low calcium prompts the parathyroid glands to release more PTH.
- Tertiary: In advanced CKD, hyperplastic and autonomous parathyroid glands cause persistent high PTH levels.
- Tertiary Hyperparathyroidism can lead to bone disease (osteitis fibrosa cystica, osteopenia, osteoporosis, pathological fractures) and calciphylaxis (vascular calcification, tissue ischemia, painful ulcers).
Hyperlipidemia:
- Low albumin levels in CKD stimulate liver lipoprotein production (LDL, VLDL), increasing risk of atherosclerosis and cardiovascular disease.
- Inflammation and endothelial dysfunction contribute to atherosclerosis.

CKD Diagnosis

GFR: GFR < 60 mL/min/1.73 m² for ≥ 3 months signifies CKD.
Albuminuria: Urine albumin-to-creatinine ratio indicates CKD severity.
- <30: Mild
- 30-300: Microalbuminuria
- 300: Macroalbuminuria
Renal Ultrasound: May show hyper-echogenicity, cortical thinning, and smaller kidney size (non-specific).
- Also identifies conditions like polycystic kidney disease (PKD), characterized by enlarged kidneys with cysts.
Urinalysis with Microscopy: Broad waxy casts indicate chronic kidney injury.

CKD Treatment

Metabolic Acidosis:
- Prevent: Low-phosphate diet.
- Treat: Phosphate binders, calcitriol (if calcium and Vitamin D low), calcium chelators, or parathyroidectomy (for tertiary hyperparathyroidism).
Hyperkalemia:
- Prevent: Low-potassium diet.
- Treat: Loop diuretics, potassium-binding resins.
Hypervolemia:
- Prevent: Sodium restriction.
- Treat: Loop diuretics.
Uremia (Waste buildup):
- Treat with dialysis (hemodialysis, peritoneal dialysis).
Secondary Hypertension:
- Treat: ACE inhibitors or ARBs.
Anemia of CKD:
- Treat: Iron supplementation (if deficient), erythropoietin (EPO) therapy.
Hyperparathyroidism:
- Prevent: Low-phosphate diet.
- Treat: Phosphate binders, calcitriol, calcium chelators, or parathyroidectomy (for tertiary hyperparathyroidism).

CKD Stage Progression

CKD Stage 3A: GFR 45-59 mL/min/1.73 m²
CKD Stage 3B: GFR 30-44 mL/min/1.73 m²
CKD Stage 4: GFR 15-29 mL/min/1.73 m²
CKD Stage 5 (End-Stage Renal Disease): GFR < 15 mL/min/1.73 m²

CKD Treatment Considerations

Iodine Contrast: Avoid in CKD patients (GFR < 60 mL/min/1.73 m²) due to contrast-induced nephropathy risk.
Gadolinium Contrast: Avoid in CKD patients (GFR < 30 mL/min/1.73 m²) due to nephrogenic systemic fibrosis risk.
Drug Dosing: Adjust medications for renal function to prevent toxicity.

Dialysis Access Options

Hemodialysis:
- AV Fistula: Preferred long-term access, low infection risk, but requires 4-6 weeks to mature.
- AV Graft: Alternative, faster maturation, higher risk of stenosis, thrombosis, and graft failure.
- Central Venous Catheter: Urgent/emergent use, high infection risk.
Peritoneal Dialysis: Uses implanted peritoneal catheter.

Dialysis Complications

Hypotension: Can occur during hemodialysis.
Dialysis Disequilibrium Syndrome: Rapid urea removal causing cerebral edema and symptoms (headache, nausea, vomiting).
Access Complications:
- Central Venous Catheters: High infection risk.
- AV Grafts: Stenosis and clotting risk.
- Peritoneal Dialysis: Peritonitis risk.

Kidney Transplantation

Considered for End-Stage Renal Disease (ESRD), typically on the left side due to longer renal vein.

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Description

This quiz covers key concepts regarding Chronic Kidney Disease (CKD), including its causes, progression, and the role of glomerulosclerosis. It also explores the impact of diabetic nephropathy on renal function and how hyperglycemia contributes to the condition. Test your understanding of CKD pathology and its implications.