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Pathology - Acute Tubular Necrosis
Caused by renal ischemia (such as prolonged low blood pressure, shock), crush injury (such hard exercise, myoglobinuria), contrast or nephrotoxic medications (such as aminoglycosides).
Kidney pathology includes focal tubular epithelial necrosis, basement membrane rupture, eosinophilic hyaline casts in collecting ducts, interstitial edema, and indications of epithelial regeneration with flattened cells and mitotic patterns.
Symptoms and signs
Exhibits symptoms of acute renal failure.
Arrhythmia-induced death due to hyperkalemia may happen in the early oliguric phase.
Laboratory results show oliguria, increased urinary sodium (> 40 mEq/L), azotemia, tubular epithelial cell casts (muddy-brown casts) in urine, and hyperkalemia.
Treatment involves the use of loop diuretics to induce diuresis and the monitoring of electrolyte and fluid levels, which may necessitate dialysis.
May result in the restoration of renal function or progress to end-stage renal failure (ESRD).
Caused by renal ischemia (such as prolonged low blood pressure, shock), crush injury (such hard exercise, myoglobinuria), contrast or nephrotoxic medications (such as aminoglycosides).
Kidney pathology includes focal tubular epithelial necrosis, basement membrane rupture, eosinophilic hyaline casts in collecting ducts, interstitial edema, and indications of epithelial regeneration with flattened cells and mitotic patterns.
Symptoms and signs
Exhibits symptoms of acute renal failure.
Arrhythmia-induced death due to hyperkalemia may happen in the early oliguric phase.
Laboratory results show oliguria, increased urinary sodium (> 40 mEq/L), azotemia, tubular epithelial cell casts (muddy-brown casts) in urine, and hyperkalemia.
Treatment involves the use of loop diuretics to induce diuresis and the monitoring of electrolyte and fluid levels, which may necessitate dialysis.
May result in the restoration of renal function or progress to end-stage renal failure (ESRD).
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Pathology - Adult Polycystic Kidney and Infantile Polycystic kidney
Adult Polycystic Kidney Disease (APKD): Autosomal dominant inheritance is observed in 90% of cases due to a mutation in the APKD1 gene located on chromosome 16.
Infantile Polycystic Kidney (IPKD) is inherited in an autosomal recessive manner.
APKD: Bilateral replacement of renal parenchyma with several big cysts of varying sizes.
IPKD refers to closed, tiny, and uniform cysts that are not connected to the collecting system.
The patient presents with hypertension, hematuria, palpable renal masses, and flank pain. A CT scan reveals numerous cysts in both kidneys. The condition is linked to secondary polycythemia, polycystic liver disease, berry aneurysms of the cerebral circulation, and mitral valve prolapse.
IPKD: CT scan reveals the presence of many cysts at birth.
APKD: Renal failure cannot be prevented by therapy, however treating hypertension with ACE inhibitors and following a low-protein diet may help slow down the progression of end-stage renal disease. Transplantation should be considered.
IPKD leads to death shortly after birth.
Adult Polycystic Kidney Disease (APKD): Autosomal dominant inheritance is observed in 90% of cases due to a mutation in the APKD1 gene located on chromosome 16.
Infantile Polycystic Kidney (IPKD) is inherited in an autosomal recessive manner.
APKD: Bilateral replacement of renal parenchyma with several big cysts of varying sizes.
IPKD refers to closed, tiny, and uniform cysts that are not connected to the collecting system.
The patient presents with hypertension, hematuria, palpable renal masses, and flank pain. A CT scan reveals numerous cysts in both kidneys. The condition is linked to secondary polycythemia, polycystic liver disease, berry aneurysms of the cerebral circulation, and mitral valve prolapse.
IPKD: CT scan reveals the presence of many cysts at birth.
APKD: Renal failure cannot be prevented by therapy, however treating hypertension with ACE inhibitors and following a low-protein diet may help slow down the progression of end-stage renal disease. Transplantation should be considered.
IPKD leads to death shortly after birth.
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Pathology - Urolithiasis ( kidney stones)
Calcium oxalate and/or calcium phosphate stones make up 80%-85% of cases. Conditions causing elevated levels of calcium in the blood include hyperparathyroidism, vitamin D toxicity, and sarcoidosis.
Struvite stones (10%) are caused by urease-positive bacteria such as Proteus vulgaris.
Uric acid stones (5%): Associated with conditions characterized by elevated cell proliferation and turnover, such as leukemia, myeloproliferative diseases, or hyperuricemia.
Cystine stones are caused by cystinuria, a genetic condition that impairs the reabsorption of cystine.
Pathology: Kidney stones found in renal calyces, pelvis, or bladder.
Urolithiasis can lead to further pathological disorders such renal colic (painful swelling of the ureter), hydronephrosis, and pyelonephritis.
Symptoms and signs
Flank pain extending to the groin and presence of blood in the urine.
Imaging: Calcium stones and struvite stones are visible on X-rays, while uric acid and cystine stones are not visible on X-rays.
Complications may involve the reappearance of calcium stones and a higher occurrence of UTIs caused by struvite.
Therapies
Many stones can be naturally passed with increased fluid intake and pain management. In other situations, surgery or lithotripsy may be required. Hydrochlorothiazide can be considered for recurring calcium stones, whereas allopurinol with alkaline diuresis may be helpful for uric acid stones.
Hydronephrosis is the enlargement of the renal pelvis and calyces. Urinary outflow obstruction causes this condition, which is linked to gradual kidney atrophy if not treated.
Calcium oxalate and/or calcium phosphate stones make up 80%-85% of cases. Conditions causing elevated levels of calcium in the blood include hyperparathyroidism, vitamin D toxicity, and sarcoidosis.
Struvite stones (10%) are caused by urease-positive bacteria such as Proteus vulgaris.
Uric acid stones (5%): Associated with conditions characterized by elevated cell proliferation and turnover, such as leukemia, myeloproliferative diseases, or hyperuricemia.
Cystine stones are caused by cystinuria, a genetic condition that impairs the reabsorption of cystine.
Pathology: Kidney stones found in renal calyces, pelvis, or bladder.
Urolithiasis can lead to further pathological disorders such renal colic (painful swelling of the ureter), hydronephrosis, and pyelonephritis.
Symptoms and signs
Flank pain extending to the groin and presence of blood in the urine.
Imaging: Calcium stones and struvite stones are visible on X-rays, while uric acid and cystine stones are not visible on X-rays.
Complications may involve the reappearance of calcium stones and a higher occurrence of UTIs caused by struvite.
Therapies
Many stones can be naturally passed with increased fluid intake and pain management. In other situations, surgery or lithotripsy may be required. Hydrochlorothiazide can be considered for recurring calcium stones, whereas allopurinol with alkaline diuresis may be helpful for uric acid stones.
Hydronephrosis is the enlargement of the renal pelvis and calyces. Urinary outflow obstruction causes this condition, which is linked to gradual kidney atrophy if not treated.
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Pathology - Metabolic Acidosis
Causes of anion-gap metabolic acidosis include renal failure, lactic acidosis, diabetic ketoacidosis, specific poisons such as methanol, paraldehyde, phenformin, cyanide, carbon monoxide, ethanol, ethylene glycol, salicylate, and INH.
Causes of normal anion-gap metabolic acidosis include traveler's diarrhea, acetazolamide overdose, glue sniffing, renal tubular acidosis, and hyperchloremic metabolic acidosis.
Pathology
Primary Disturbance: Reduction in HCO3 levels.
Compensatory response: Reduction in Pco2 causes vasodilation and reduced cardiac contractility (insensitive to catecholamines), potentially resulting in shock.
Symptoms and signs
Hyperventilation or Kussmaul breathing (deep, sighing respirations); other signs and symptoms vary based on the underlying etiology of metabolic acidosis.
Laboratory results: pH, pc02, and HCO3 levels have reduced.
Therapy
Administer bicarbonate if pH is below 7.1, address the root cause, and closely observe fluid volume and electrolyte levels.
Calculation of anion gap: Anion gap is calculated by subtracting the sum of chloride and bicarbonate ions from the sodium ion concentration. The usual range for anion gap is 6-12 mEq/L, and it increases when an unmeasured anion replaces HC03-.
Compensation computation using Winter's formula: The decrease in PCO2 can be calculated using the formula: 1.5(HCO3-) + 8 ± 2.
Causes of anion-gap metabolic acidosis include renal failure, lactic acidosis, diabetic ketoacidosis, specific poisons such as methanol, paraldehyde, phenformin, cyanide, carbon monoxide, ethanol, ethylene glycol, salicylate, and INH.
Causes of normal anion-gap metabolic acidosis include traveler's diarrhea, acetazolamide overdose, glue sniffing, renal tubular acidosis, and hyperchloremic metabolic acidosis.
Pathology
Primary Disturbance: Reduction in HCO3 levels.
Compensatory response: Reduction in Pco2 causes vasodilation and reduced cardiac contractility (insensitive to catecholamines), potentially resulting in shock.
Symptoms and signs
Hyperventilation or Kussmaul breathing (deep, sighing respirations); other signs and symptoms vary based on the underlying etiology of metabolic acidosis.
Laboratory results: pH, pc02, and HCO3 levels have reduced.
Therapy
Administer bicarbonate if pH is below 7.1, address the root cause, and closely observe fluid volume and electrolyte levels.
Calculation of anion gap: Anion gap is calculated by subtracting the sum of chloride and bicarbonate ions from the sodium ion concentration. The usual range for anion gap is 6-12 mEq/L, and it increases when an unmeasured anion replaces HC03-.
Compensation computation using Winter's formula: The decrease in PCO2 can be calculated using the formula: 1.5(HCO3-) + 8 ± 2.
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Pathology - Metabolic Alkalosis
Etiology
Saline-responsive metabolic alkalosis is induced by a decrease in extracellular volume resulting from vomiting, diuretic usage, or posthypercapnia alkalosis.
Saline-resistant metabolic alkalosis is typically caused by an excess of mineralocorticoids (such as in Conn syndrome, renovascular disease, or Cushing disease), use of alkalis with reduced glomerular filtration rate (e.g., antacids), or severe hypokalemia.
Pathology
Main issue: Elevated levels of HCO3.
Compensatory response: Hypoventilation leads to an increase in Pco2 to elevate bicarbonate concentration.
Symptoms and Signs
Metabolic alkalosis is typically linked with hypokalemia, which exacerbates the condition by enhancing bicarbonate absorption in the proximal tubule and hydrogen ion release in the distal tubule.
May manifest with symptoms of dehydration such as sunken eyes, reduced skin elasticity, tiredness, low blood pressure, and muscle weakness due to low potassium levels. It can also lead to reduced blood flow to the brain and irregular heartbeats.
Laboratory results: Elevated pH, elevated Pco2, elevated HCO3, low potassium levels.
Therapy
Saline-responsive: Replenishment of fluids and electrolytes.
Treat the root cause of excess mineralocorticoid and replenish potassium to address saline resistance.
Remuneration: An rise of 1 mEq/L in HCO3 results in a 0.7 mm Hg increase in pCO2.
Etiology
Saline-responsive metabolic alkalosis is induced by a decrease in extracellular volume resulting from vomiting, diuretic usage, or posthypercapnia alkalosis.
Saline-resistant metabolic alkalosis is typically caused by an excess of mineralocorticoids (such as in Conn syndrome, renovascular disease, or Cushing disease), use of alkalis with reduced glomerular filtration rate (e.g., antacids), or severe hypokalemia.
Pathology
Main issue: Elevated levels of HCO3.
Compensatory response: Hypoventilation leads to an increase in Pco2 to elevate bicarbonate concentration.
Symptoms and Signs
Metabolic alkalosis is typically linked with hypokalemia, which exacerbates the condition by enhancing bicarbonate absorption in the proximal tubule and hydrogen ion release in the distal tubule.
May manifest with symptoms of dehydration such as sunken eyes, reduced skin elasticity, tiredness, low blood pressure, and muscle weakness due to low potassium levels. It can also lead to reduced blood flow to the brain and irregular heartbeats.
Laboratory results: Elevated pH, elevated Pco2, elevated HCO3, low potassium levels.
Therapy
Saline-responsive: Replenishment of fluids and electrolytes.
Treat the root cause of excess mineralocorticoid and replenish potassium to address saline resistance.
Remuneration: An rise of 1 mEq/L in HCO3 results in a 0.7 mm Hg increase in pCO2.
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Pathology - Respiratory Acidosis
Resulting from acute lung disease such as ARDS and airway obstruction, chronic lung disease like COPD, CNS depression caused by opioids, sedatives, and narcotics, or weakened respiratory muscles due to conditions like ALS, kyphoscoliosis, MS, and polio.
Primary issue: Elevated Pco2 levels (hypercapnia) due to reduced alveolar ventilation.
Compensatory response: HCO3 increases due to enhanced renal HCO3 reabsorption triggered by low pH and high Pco2.
Symptoms include hypoventilation, drowsiness, cognitive impairment, muscle jerks with hand flapping, and indications of elevated pressure within the skull (such as swollen optic nerves and a condition resembling a brain tumor).
Laboratory results: pH decreased, Pco2 increased, HCO3 increased.
Address the root cause of acute respiratory acidosis and consider using short-term mechanical ventilation to assist with breathing.
No intervention required for persistent respiratory acidosis.
Acute compensation occurs with a 1 mEq/L increase in bicarbonate for every 10 mm Hg increase in partial pressure of carbon dioxide.
Chronic compensation occurs with a 3.5 mEq/L rise in HCO3 for every 10-mm Hg increase in PCO2.
Resulting from acute lung disease such as ARDS and airway obstruction, chronic lung disease like COPD, CNS depression caused by opioids, sedatives, and narcotics, or weakened respiratory muscles due to conditions like ALS, kyphoscoliosis, MS, and polio.
Primary issue: Elevated Pco2 levels (hypercapnia) due to reduced alveolar ventilation.
Compensatory response: HCO3 increases due to enhanced renal HCO3 reabsorption triggered by low pH and high Pco2.
Symptoms include hypoventilation, drowsiness, cognitive impairment, muscle jerks with hand flapping, and indications of elevated pressure within the skull (such as swollen optic nerves and a condition resembling a brain tumor).
Laboratory results: pH decreased, Pco2 increased, HCO3 increased.
Address the root cause of acute respiratory acidosis and consider using short-term mechanical ventilation to assist with breathing.
No intervention required for persistent respiratory acidosis.
Acute compensation occurs with a 1 mEq/L increase in bicarbonate for every 10 mm Hg increase in partial pressure of carbon dioxide.
Chronic compensation occurs with a 3.5 mEq/L rise in HCO3 for every 10-mm Hg increase in PCO2.
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Pathology - Respiratory alkalosis
Acute respiratory alkalosis is triggered by hyperventilation and can also be caused by several conditions such as salicylate overdose, pneumonia, sepsis, pregnancy, pulmonary edema, pulmonary embolism, or cirrhosis.
Chronic respiratory alkalosis is induced by elevated altitudes or pregnancy.
Main issue: Reduction in Pco2 levels- Compensatory response: Reduction in bicarbonate levels due to heightened production of nitric acid in the kidneys.
Symptoms of acute respiratory alkalosis include reduced cerebral blood flow leading to light-headedness, anxiety, paresthesias, numbness around the mouth, tingling in the extremities, and hyperventilation. It may also result in cardiac arrhythmias.
Laboratory results show elevated pH, reduced Pco2, and decreased HCO3 levels.
Treat acute hyperventilation syndrome caused by worry by breathing into a paper bag to boost Pco2. Otherwise, address the underlying cause such as sepsis or pneumonia.
Acute compensation involves a reduction of 2 mEq/L of bicarbonate for every 10-mm Hg decrease in carbon dioxide pressure.
Chronic compensation occurs with a drop of 5 mEq/L in bicarbonate for every 10-mm Hg fall in Pco2.
Acute respiratory alkalosis is triggered by hyperventilation and can also be caused by several conditions such as salicylate overdose, pneumonia, sepsis, pregnancy, pulmonary edema, pulmonary embolism, or cirrhosis.
Chronic respiratory alkalosis is induced by elevated altitudes or pregnancy.
Main issue: Reduction in Pco2 levels- Compensatory response: Reduction in bicarbonate levels due to heightened production of nitric acid in the kidneys.
Symptoms of acute respiratory alkalosis include reduced cerebral blood flow leading to light-headedness, anxiety, paresthesias, numbness around the mouth, tingling in the extremities, and hyperventilation. It may also result in cardiac arrhythmias.
Laboratory results show elevated pH, reduced Pco2, and decreased HCO3 levels.
Treat acute hyperventilation syndrome caused by worry by breathing into a paper bag to boost Pco2. Otherwise, address the underlying cause such as sepsis or pneumonia.
Acute compensation involves a reduction of 2 mEq/L of bicarbonate for every 10-mm Hg decrease in carbon dioxide pressure.
Chronic compensation occurs with a drop of 5 mEq/L in bicarbonate for every 10-mm Hg fall in Pco2.
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Pathology - Rapidly Progressive (Crescentic) Glomerulonephritis
Type 1: Idiopathic or Goodpasture syndrome.
Type 2 (immune complex) glomerulonephritis can be caused by idiopathic factors, postinfectious conditions, systemic lupus erythematosus (SLE), IgA nephropathy, and Henoch-Schonlein purpura.
Category 3 (pauci-immune type): Conditions include idiopathic, Wegener granulomatosis, and microscopic polyangiitis.
Pathology
Light microscopy shows the formation of a crescent-moon shape between the Bowman capsule and glomerular tuft. This is caused by the deposition of fibrin in the Bowman space and the proliferation of parietal epithelial cells of the Bowman capsule.
Clinical Symptoms
Presence of nephritic syndrome characterized by hematuria, hypertension, and azotemia.
Signs and symptoms vary depending on the cause, such as hemoptysis and anti-GBM antibodies in Goodpasture syndrome.
Therapy
Administer diuretics and ACE inhibitors; consider immunosuppression with steroids or cytotoxic medicines based on the underlying reason; dialysis or transplant may be necessary.
Patients typically progress quickly to end-stage renal failure necessitating dialysis.
Rapidly progressive glomerulonephritis (RPGN) is a condition characterized by significant and advancing damage to the glomeruli. It includes various causes.
Type 1: Idiopathic or Goodpasture syndrome.
Type 2 (immune complex) glomerulonephritis can be caused by idiopathic factors, postinfectious conditions, systemic lupus erythematosus (SLE), IgA nephropathy, and Henoch-Schonlein purpura.
Category 3 (pauci-immune type): Conditions include idiopathic, Wegener granulomatosis, and microscopic polyangiitis.
Pathology
Light microscopy shows the formation of a crescent-moon shape between the Bowman capsule and glomerular tuft. This is caused by the deposition of fibrin in the Bowman space and the proliferation of parietal epithelial cells of the Bowman capsule.
Clinical Symptoms
Presence of nephritic syndrome characterized by hematuria, hypertension, and azotemia.
Signs and symptoms vary depending on the cause, such as hemoptysis and anti-GBM antibodies in Goodpasture syndrome.
Therapy
Administer diuretics and ACE inhibitors; consider immunosuppression with steroids or cytotoxic medicines based on the underlying reason; dialysis or transplant may be necessary.
Patients typically progress quickly to end-stage renal failure necessitating dialysis.
Rapidly progressive glomerulonephritis (RPGN) is a condition characterized by significant and advancing damage to the glomeruli. It includes various causes.
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Pathology - Alport Syndrome
X-linked dominant genetic condition characterized by a mutation in the alpha 5-chain of type IV collagen.
Pathology
Electron microscopy shows irregular areas of thickening or thinning in the glomerular basement membrane with longitudinal breaking of the lamina densa.
Clinical Symptoms and Signs
The combination of nephritis, nerve deafness, and eye problems such as cataracts, lens displacement, and corneal dystrophy may present initially with hematuria and erythrocyte casts.
Treatment: ACE inhibitors; kidney transplant may be considered for severe instances.
X-linked dominant genetic condition characterized by a mutation in the alpha 5-chain of type IV collagen.
Pathology
Electron microscopy shows irregular areas of thickening or thinning in the glomerular basement membrane with longitudinal breaking of the lamina densa.
Clinical Symptoms and Signs
The combination of nephritis, nerve deafness, and eye problems such as cataracts, lens displacement, and corneal dystrophy may present initially with hematuria and erythrocyte casts.
Treatment: ACE inhibitors; kidney transplant may be considered for severe instances.
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Pathology - Membranoproliferative Glomerulonephritis
Linked to hereditary lack of complement components.
Type I is observed in systemic lupus erythematosus, hepatitis B and C, and entails activation of both the conventional and alternative pathways.
Type II specifically entails the activation of the alternative route exclusively.
The majority of affected patients are under 30 years old.
Types I and II: Under light microscopy, the basement membrane shows reduplication (splitting) and the mesangial matrix expands into the capillary loops, creating a tram track appearance.
Type I: Electron microscopy reveals electron-dense deposits located beneath the endothelium.
Type II: Electron microscopy reveals a distinct dense deposit of uniform material within the glomerular basement membrane.
Clinical Symptoms
Type I typically manifests with nephrotic syndrome.
Type II typically manifests as nephritic syndrome characterized by hematuria and persistent renal failure.
Laboratory results: Reduced C3 levels, increased BUN and Cr, presence of RBCs and/or RBC casts in urine.
Treatment include corticosteroids and immunosuppression if deemed suitable for the root cause.
Prognosis involves gradual progression to renal failure with a high likelihood of recurrence post-transplant.
Notes
Linked to hereditary lack of complement components.
Type I is observed in systemic lupus erythematosus, hepatitis B and C, and entails activation of both the conventional and alternative pathways.
Type II specifically entails the activation of the alternative route exclusively.
The majority of affected patients are under 30 years old.
Types I and II: Under light microscopy, the basement membrane shows reduplication (splitting) and the mesangial matrix expands into the capillary loops, creating a tram track appearance.
Type I: Electron microscopy reveals electron-dense deposits located beneath the endothelium.
Type II: Electron microscopy reveals a distinct dense deposit of uniform material within the glomerular basement membrane.
Clinical Symptoms
Type I typically manifests with nephrotic syndrome.
Type II typically manifests as nephritic syndrome characterized by hematuria and persistent renal failure.
Laboratory results: Reduced C3 levels, increased BUN and Cr, presence of RBCs and/or RBC casts in urine.
Treatment include corticosteroids and immunosuppression if deemed suitable for the root cause.
Prognosis involves gradual progression to renal failure with a high likelihood of recurrence post-transplant.
Notes
