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Pathology - Renal Cell Carcinoma
Linked to von Hippel-Lindau disease, deletion on chromosome 3, and cigarette smoking.
Most prevalent in men with a 2:1 male to female ratio during their sixth decade of life, typically between the ages of 50 and 70.
The kidney pathology is characterized by polygonal transparent cells that are formed from the tubular epithelium and are defined solely by cell membranes with nuclei pushed to the sides.
Invades the inferior vena cava and spreads through the bloodstream to the lungs, bones, and other locations.
Clinical Symptoms and Signs
Characterized by hematuria, palpable abdominal mass, flank pain, prolonged fever, and weight loss; linked with paraneoplastic disorders such as ectopic EPO, ACTH, PTHrP, prolactin, gonadotropins, and renin.
Imaging: CT scan shows a solid mass in the kidney.
Laboratory results: Secondary polycythemia caused by elevated erythropoietin (EPO) levels.
Perform radical nephrectomy for localized disease and administer chemotherapy or radiation for invasive or distant disease.
Renal cell carcinoma is the most prevalent type of kidney cancer.
Linked to von Hippel-Lindau disease, deletion on chromosome 3, and cigarette smoking.
Most prevalent in men with a 2:1 male to female ratio during their sixth decade of life, typically between the ages of 50 and 70.
The kidney pathology is characterized by polygonal transparent cells that are formed from the tubular epithelium and are defined solely by cell membranes with nuclei pushed to the sides.
Invades the inferior vena cava and spreads through the bloodstream to the lungs, bones, and other locations.
Clinical Symptoms and Signs
Characterized by hematuria, palpable abdominal mass, flank pain, prolonged fever, and weight loss; linked with paraneoplastic disorders such as ectopic EPO, ACTH, PTHrP, prolactin, gonadotropins, and renin.
Imaging: CT scan shows a solid mass in the kidney.
Laboratory results: Secondary polycythemia caused by elevated erythropoietin (EPO) levels.
Perform radical nephrectomy for localized disease and administer chemotherapy or radiation for invasive or distant disease.
Renal cell carcinoma is the most prevalent type of kidney cancer.
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Pathology - Transitional Cell Carcinoma
Linked to smoking, alcohol consumption, exposure to aniline dyes, previous cyclophosphamide therapy, and phenacetin misuse.
Most prevalent among males over the age of 40.
The pathology of this condition ranges from flat to papillary and from noninvasive to invasive. It can develop in any part of the urinary tract system (renal calyces, renal pelvis, ureters, bladder) and may extend to adjacent tissue through local extension.
Microscopic examination reveals several stages of carcinoma, ranging from well-differentiated tumor cells similar to normal transitional cells to anaplastic tumor cells with large cells and numerous mitoses.
Typically manifests as painless blood in the urine; may also show signs of irritative voiding symptoms (if there is a concurrent infection), a detectable mass during a bimanual examination, enlarged liver, or swollen lymph nodes above the collarbone (if it has spread).
Treatment for bladder cancer may involve chemotherapy, radiation, transurethral resection, or radical cystectomy, as the cancer often recurs after removal.
Prognosis relies on the stage and grade of the condition.
Squamous cell carcinoma (SCC) of the bladder makes up 3%-7% of bladder malignancies in the United States and is linked to schistosomiasis and other factors causing persistent bladder infection.
Linked to smoking, alcohol consumption, exposure to aniline dyes, previous cyclophosphamide therapy, and phenacetin misuse.
Most prevalent among males over the age of 40.
The pathology of this condition ranges from flat to papillary and from noninvasive to invasive. It can develop in any part of the urinary tract system (renal calyces, renal pelvis, ureters, bladder) and may extend to adjacent tissue through local extension.
Microscopic examination reveals several stages of carcinoma, ranging from well-differentiated tumor cells similar to normal transitional cells to anaplastic tumor cells with large cells and numerous mitoses.
Typically manifests as painless blood in the urine; may also show signs of irritative voiding symptoms (if there is a concurrent infection), a detectable mass during a bimanual examination, enlarged liver, or swollen lymph nodes above the collarbone (if it has spread).
Treatment for bladder cancer may involve chemotherapy, radiation, transurethral resection, or radical cystectomy, as the cancer often recurs after removal.
Prognosis relies on the stage and grade of the condition.
Squamous cell carcinoma (SCC) of the bladder makes up 3%-7% of bladder malignancies in the United States and is linked to schistosomiasis and other factors causing persistent bladder infection.
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Pathology - Wilms Tumor
Resulting from the loss of the WT-1 gene, a tumor suppressor, located on the short arm of chromosome 11.
Typically observed in young children aged 2 to 5.
Pathology: A sizable, single, clearly defined mass in the kidney that arises from primitive metanephric tissue.
Microscopic examination reveals immature stroma with primitive tubules and glomeruli, along with mesenchymal features such as bone, cartilage, and connective tissue.
Clinical Symptoms
Typically appears as a large, painless lump in the side or abdomen of a young child; may also come with fever or stomach pain; can be linked to one-sided muscle enlargement (hemihypertrophy).
Laboratory results: Microscopic presence of blood in urine.
Tumor removal surgery followed by radiation and chemotherapy with actinomycin D and vincristine.
The survival rate is great.
Wilms tumor may be linked with the WAGR complex, which includes Wilms tumor, aniridia (lack of iris), genitourinary malformation, and mental-motor retardation.
Resulting from the loss of the WT-1 gene, a tumor suppressor, located on the short arm of chromosome 11.
Typically observed in young children aged 2 to 5.
Pathology: A sizable, single, clearly defined mass in the kidney that arises from primitive metanephric tissue.
Microscopic examination reveals immature stroma with primitive tubules and glomeruli, along with mesenchymal features such as bone, cartilage, and connective tissue.
Clinical Symptoms
Typically appears as a large, painless lump in the side or abdomen of a young child; may also come with fever or stomach pain; can be linked to one-sided muscle enlargement (hemihypertrophy).
Laboratory results: Microscopic presence of blood in urine.
Tumor removal surgery followed by radiation and chemotherapy with actinomycin D and vincristine.
The survival rate is great.
Wilms tumor may be linked with the WAGR complex, which includes Wilms tumor, aniridia (lack of iris), genitourinary malformation, and mental-motor retardation.
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Pathology - Prolactinoma
Pituitary lactotroph adenoma is the most prevalent type of pituitary tumor that causes this condition.
Pituitary adenoma consists of many chromophobic cells that contain secretory granules filled with prolactin.
Hyperprolactinemia causes reduced levels of LH and FSH by feedback inhibition, leading to amenorrhea and infertility.
Symptoms and signs
Absence of menstruation in women or erectile dysfunction in males; inability to conceive; spontaneous flow of milk from the breasts.
Bitemporal hemianopsia or other visual abnormalities may occur due to potential compression of the optic chiasm by an adenoma.
Laboratory results: Reduced LH and FSH, elevated prolactin levels.
Treatment: Bromocriptine is used as a dopamine analog to inhibit prolactin secretion.
Adenoma removal with surgery or radiation.
Hyperprolactinemia can result from estrogen therapy, hypothyroidism, medications that affect dopamine secretion (such as methyl-dopa, reserpine, antipsychotic medicines), hypothalamic abnormalities, or renal insufficiency.
Pituitary lactotroph adenoma is the most prevalent type of pituitary tumor that causes this condition.
Pituitary adenoma consists of many chromophobic cells that contain secretory granules filled with prolactin.
Hyperprolactinemia causes reduced levels of LH and FSH by feedback inhibition, leading to amenorrhea and infertility.
Symptoms and signs
Absence of menstruation in women or erectile dysfunction in males; inability to conceive; spontaneous flow of milk from the breasts.
Bitemporal hemianopsia or other visual abnormalities may occur due to potential compression of the optic chiasm by an adenoma.
Laboratory results: Reduced LH and FSH, elevated prolactin levels.
Treatment: Bromocriptine is used as a dopamine analog to inhibit prolactin secretion.
Adenoma removal with surgery or radiation.
Hyperprolactinemia can result from estrogen therapy, hypothyroidism, medications that affect dopamine secretion (such as methyl-dopa, reserpine, antipsychotic medicines), hypothalamic abnormalities, or renal insufficiency.
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Pathology - Pituitary Cachexia
Sheehan syndrome is typically caused by pituitary adenomas, ischemic necrosis of the anterior pituitary after postpartum hemorrhage, pituitary surgery, pituitary radiotherapy, or pituitary damage.
Adenoma is a defined growth made up of uniform, polygonal cells.
Sheehan syndrome is characterized by an early hemorrhagic lesion in the anterior pituitary that eventually resolves into a tiny fibrous band.
Generalized panhypopituitarism presents as hypothyroidism (low TSH), hypogonadism with infertility (low LH and FSH), hypocortisolism (low ACTH), reduced prolactin, and decreased growth hormone.
Bitemporal hemianopsia may occur if caused by adenoma, resulting from the compression of the optic chiasm.
Laboratory results: Low blood sugar; low sodium levels; reduced levels of estrogen, testosterone, and progesterone; lowered cortisol; decreased T4.
Treatment options include hormone replacement therapy and surgical excision of the adenoma.
Pituitary adenomas can lead to hyperpituitarism and may be linked to MEN type I syndrome.
Sheehan syndrome is typically caused by pituitary adenomas, ischemic necrosis of the anterior pituitary after postpartum hemorrhage, pituitary surgery, pituitary radiotherapy, or pituitary damage.
Adenoma is a defined growth made up of uniform, polygonal cells.
Sheehan syndrome is characterized by an early hemorrhagic lesion in the anterior pituitary that eventually resolves into a tiny fibrous band.
Generalized panhypopituitarism presents as hypothyroidism (low TSH), hypogonadism with infertility (low LH and FSH), hypocortisolism (low ACTH), reduced prolactin, and decreased growth hormone.
Bitemporal hemianopsia may occur if caused by adenoma, resulting from the compression of the optic chiasm.
Laboratory results: Low blood sugar; low sodium levels; reduced levels of estrogen, testosterone, and progesterone; lowered cortisol; decreased T4.
Treatment options include hormone replacement therapy and surgical excision of the adenoma.
Pituitary adenomas can lead to hyperpituitarism and may be linked to MEN type I syndrome.
Sheehan Syndrome
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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.
