Chapter 8 - Renal Disease
Symptoms usually occur in children and young adults following respiratory infections caused by certain strains of group A streptococcus that contain M protein in the cell wall.
They form immune complexes with their corresponding circulating antibodies and become deposited on the glomerular membranes.
Demonstration of an elevated serum antistreptolysin O (ASO) titer or anti–group A streptococcal enzyme tests provide evidence that the disease is of streptococcal origin.
It does not produce permanent damage after treatment.
However, microscopic hematuria lasts until the membrane damage has been repaired.
Symptoms are initiated by deposition of immune complexes in the glomerulus from glomerulonephritis or an immune systemic disorder.
Macrophages migrate to the capillary walls and damage them, releasing cells and plasma into Bowman’s space and producing crescentic formations containing macrophages, fibroblasts and polymerized fibrin, causing permanent damage to the capillary tufts eventually leading to renal failure.
After viral respiratory infections, antiglomerular basement membrane antibodies are formed and attach to the basement membrane, causing capillary destruction.
Antineutrophilic cytoplasmic antibody (ANCA) bind to the neutrophils located in the vascular walls, causing granuloma formation.
It is a disease occurring primarily in children following upper respiratory infections.
Complete recovery with normal renal function is seen in more than 50% of patients while others progress to a more serious form of glomerulonephritis and renal failure.
It is characterized by pronounced thickening of the glomerular basement membrane resulting from the deposition of immunoglobulin G immune complexes.
It is associated with disorders such as systemic lupus erythematosus, Sjögren syndrome, secondary syphilis, hepatitis B, gold and mercury treatments, malignancy and even disorders of unknown origin.
It may be of two types which alters the cellularity of the glomerulus and peripheral capillaries.
Type 1 displays increased cellularity in the subendothelial cells of the mesangium (interstitial area of Bowman’s capsule), causing thickening of the capillary walls and progressing to nephrotic syndrome.
Type 2 displays extremely dense deposits in the glomerular basement membrane and progresses to chronic glomerulonephritis.
Many of the patients are children, and the disease has a poor prognosis.
It is characterized by IgA deposits in the glomerular membrane caused by increased levels in the serum as a result of mucosal infections.
The disorder is most frequently seen in children and young adults.
A patient with the disorder may remain essentially asymptomatic for 20 years or more with periodic recurrences of macroscopic hematuria; however, there is a gradual progression to chronic glomerulonephritis and end-stage renal disease.
It is usually a progression of glomerular disorders in which the permeability of the glomerular membrane is increased due to damage and changes in the electrical charges in the basal lamina and podocytes, producing a less tightly connected barrier.
This makes high-molecular-weight proteins and lipids that are normally filtered enter the urine, specifically albumin.
Albumin is depleted from the circulation, stimulating the increased production of lipids by the liver and lowering the oncotic pressure in the capillaries.
It causes fluid loss into the interstitial spaces and sodium retention, resulting in edema.
Depletion of immunoglobulins and coagulation factors places patients at an increased risk of infection and coagulation disorders.
Acute onset of the disorder can occur in instances of circulatory disruption, producing systemic shock that decrease the pressure and flow of blood to the kidney and progressing to tubular and glomerular damage that causes chronic renal failure.
Though there is little cellular change in the glomerulus, the podocytes appear to be less fitted, hampering filtration of protein.
Although the etiology is unknown at this time, allergic reactions, recent immunization, and possession of the human leukocyte antigen-B12 (HLA-B12) antigen have been associated, and it usually affects children.
The disorder responds well to corticosteroids, and prognosis is generally good, with frequent complete remissions.
It affects only certain numbers and areas of glomeruli, and the others remain normal.
Immune deposits are a frequent finding and can be seen in undamaged glomeruli.
It is often seen in association with abuse of heroin and analgesics and with AIDS.
It is a sex-linked or autosomal inherited disorder affecting the glomerular basement membrane.
Males are frequently more severely affected than females, and it progresses from the age of six during respiratory infections.
The glomerular basement membrane has a lamellated appearance with areas of thinning but there are no glomerular antibodies.
It is the most common cause of end-stage renal disease.
It involves damage to the glomerular membrane from glomerular membrane thickening, increased proliferation of mesangial cells and increased deposition of cellular and noncellular material within the glomerular matrix.
This is believed to be associated with deposition of glycosylated proteins resulting from poorly controlled blood glucose levels.
The vascular structure of the glomerulus also develops sclerosis.
This is caused by decreased blood flow leading to insufficient oxygen (ischemia), by the presence of toxic substances in the urinary filtrate, or by disorders such as shock, trauma and surgery.
Examples of toxic substances include aminoglycoside antibiotics, amphotericin B, cyclosporine, radiographic dye, organic solvents such as ethylene glycol, heavy metals, and toxic mushrooms.
Examples of conditions that may cause shock are cardiac failures, sepsis involving toxogenic bacteria, anaphylaxis, massive hemorrhage, and contact with high-voltage electricity.
Correction of the ischemia and removal of toxic substances followed by effective management of the accompanying symptoms of acute renal failure frequently result in a complete recovery.
It refers to a generalized failure of tubular reabsorption in the proximal convoluted tubule.
Therefore, substances most noticeably affected include glucose, amino acids, phosphorous, sodium, potassium, bicarbonate, and water.
Tubular reabsorption may be affected by dysfunction of the transport of filtered substances across the tubular membranes, disruption of cellular energy needed for transport or changes in the tubular membrane permeability.
It may be inherited or acquired through exposure to toxic agents such as heavy metals, outdated tetracycline or through complications of multiple myeloma and renal transplant.
It refers to the inability of the renal tubules to respond to ADH, leading to excessive excretion of urine.
It can be inherited as a sexlinked recessive gene, accquired from medications including lithium and amphotericin B, or a complication of polycystic kidney disease and sickle cell anemia.
This occurs when the maximal tubular reabsorption capacity (Tm) for glucose is reached and it can no longer be removed from the urine.
The disorder is inherited as an autosomal recessive trait, and in this case, either the number of glucose transporters in the tubules is decreased or the affinity of the transporters for glucose is decreased.
Infection may involve the lower urinary tract (urethra and bladder) or the upper urinary tract (renal pelvis, tubules, and interstitium).
Most frequently encountered is infection of the bladder (cystitis), which if untreated can progress to a more serious upper UTI.
Cystitis is seen more often in women and children who present with symptoms of urinary frequency and burning.
It refers to the infection of the upper urinary tract, including both the tubules and interstitium.
Acute pyelonephritis most frequently occurs as a result of ascending movement of bacteria from a lower UTI into the renal tubules and interstitium.
The ascending movement of bacteria from the bladder is enhanced with conditions that interfere with the downward flow of urine such as renal calculi, pregnancy and reflux of urine from the bladder back into the ureters (visicoureteral reflux).
A relatively high correlation between acute pylonephritis and bacteremia has been demonstrated, suggesting the need to perform blood cultures in addition to urine cultures.
With appropriate antibiotic therapy and removal of any underlying conditions, acute pyelonephritis can be resolved without permanent damage to the tubules.
It is a progression that results in permanent damage to the renal tubules and possible progression to chronic renal failure.
The most frequent cause is congenital urinary structural defects producing a reflux nephropathy that affects the emptying of the collecting ducts.
It is often diagnosed in children and may not be suspected until tubular damage has become advanced.
It refers to the inflammation of the renal interstitium followed by inflammation of the renal tubules.
It is primarily associated with an allergic reaction to medications that occurs within the renal interstitium, possibly caused by binding of the medication to the interstitial protein.
Symptoms tend to develop approximately 2 weeks following administration of medication.
Medications commonly associated with AIN include penicillin, methicillin, ampicillin, cephalosporins, sulfonamides, NSAIDs, and thiazide diuretics.
Discontinuation of the offending medication, administration of steroids to control the inflammation and supportive renal dialysis frequently results in a return to normal renal function.
It exists in both acute and chronic forms and may be a gradual progression from the original disorder to chronic renal failure or end-stage renal disease.
Acute renal failure (ARF), in contrast to chronic renal failure, exhibits a sudden loss of renal function and is frequently reversible.
Primary causes of ARF include a sudden decrease in blood flow to the kidney (prerenal), acute glomerular and tubular disease (renal), and renal calculi or tumor obstructions (postrenal).
The presence of RTE cells and casts suggests ATN of prerenal origin; RBCs indicate glomerular injury; WBC casts with or without bacteria indicate interstitial infection or inflammation of renal origin; and postrenal obstruction may show normal and abnormal appearing urothelial cells possibly associated with malignancy.
It refers to the formation of renal calculi of various sizes that may cause obstruction to urinary flow.
Conditions favoring the formation of renal calculi are similar to those favoring formation of urinary crystals, including pH, chemical concentration, and urinary stasis.
Analysis of the chemical composition of renal calculi plays an important role in patient management.
Analysis can be performed chemically, but examination using x-ray crystallography provides a more comprehensive analysis.
Approximately 75% of the renal calculi are composed of calcium oxalate or phosphate.
Magnesium ammonium phosphate (stuvite), uric acid, and cystine are the other primary calculi constituents.
Uric acid calculi may be associated with increased intake of foods with high purine content, so the urine pH is acidic.
Most cystine calculi are seen in conjunction with hereditary disorders of cystine metabolism.
Calcium calculi are frequently associated with metabolic calcium and phosphate disorders and occasionally diet.
Magnesium ammonium phosphate calculi are frequently accompanied by urinary infections involving urea-splitting bacteria, so the urine pH is often higher than 7.0.
It is addressed by using lithotripsy, a procedure that breaks the stones using high-energy shock waves, or surgical removal.
Patient management techniques include maintaining the urine at a pH incompatible with crystallization of the particular chemicals, maintaining adequate hydration to lower chemical concentration, and suggesting possible dietary restrictions.
Disease | Symptoms | Physical Findings | Chemical Findings | Microscopic Findings |
|---|---|---|---|---|
Acute Poststreptococcal Glomerulonephritis (AGN) | sudden onset of fever, edema around the eyes, fatigue and hypertension | oliguria | hematuria, proteinuria increased BUN | RBC casts, dysmorphic RBCs, hyaline and granular casts and WBCs |
Rapidly Progressive (Crescentic) Glomerulonephritis (RPGN) | progression of AGN, renal failure | oliguria | hematuria, proteinuria, increased BUN, fibrin degradation products, cryoglobulins and IgA immune complexes | RBC casts, dysmorphic RBCs, hyaline and granular casts and WBCs |
Goodpasture syndrome | hemoptysis (spitting out blood from lungs) and dyspnea (shortness of breath) | hematuria, proteinuria, presence of antiglomerular basement membrane antibodies in blood serum | RBC casts | |
Wegener’s Granulomatosis | pulmonary symptoms, granulomas in the small blood vessels of the kidney and respiratory system | hematuria, proteinuria, presence of antineutrophilic cytoplasmic antibody (ANCA) in the blood serum, elevated serum creatinine and BUN | RBC casts | |
Henoch-Schönlein Pupura | raised red patches on the skin, blood in the sputum and stools, progression to glomerulonephritis and renal failure | mild to heavy proteinuria and hematuria | RBC casts | |
Membranous Glomerulonephritis | nephrotic syndrome symptoms and thrombosis, slow progression with possible remission | microscopic hematuria and proteinuria | ||
Membranoproliferative Glomerulonephritis | autoimmune disorders, infections and malignancies. | hematuria and proteinuria, decreased blood serum complement levels | ||
Immunogloblin A Nephropathy/Berger Disease | progression of glomerular disorders, fatigue, anemia, hypertension and edema | oliguria | macroscopic hematuria, proteinuria, glucosuria, markedly decreased glomerular filtration rate, increased BUN and creatinine, electrolyte imbalance, increased serum IgA levels | many varieties of casts including broad casts |
Nephrotic Syndrome | pronounced edema | massive proteinuria (greater than 3.5 g/d), microscopic hematuria, low serum albumin and high serum lipids | urinary fat droplets, oval fat bodies, RTE cells; and epithelial, fatty, and waxy casts | |
Minimal Change Disease/Lipid Nephropathy | edema | heavy proteinuria, transient hematuria | ||
Focal Segmental Glomerulosclerosis (FSGS) | edema | immunoglobulins M and C3, moderate to heavy proteinuria and microscopic hematuria | ||
Alport Syndrome | abnormalities in hearing and vision from the age of six, renal insufficiency in later life, progression to nephrotic syndrome and end-stage renal disease | macroscopic and microscopic hematuria | ||
Diabetic Nephropathy/Kimmelstiel-Wilson Disease | ||||
Acute Tubular Necrosis (ATN) | mild proteinuria and microscopic hematuria | RTE cells and RTE cell casts containing tubular fragments consisting of three or more cells; hyaline casts, granular casts, waxy casts and broad casts | ||
Fanconi Syndrome | glycosuria and possible mild proteinuria | |||
Nephrogenic Diabetes Insipidus | low specific gravity and pale yellow color | possible false-negative results for chemical test | ||
Renal Glycosuria | ||||
Urinary Tract Infection (UTI) | mild proteinuria and hematuria, increased pH | numerous WBCs and bacteria | ||
Acute Pyelonephritis | increased urinary frequency, burning sensation while urinating and lower back pain | mild proteinuria and hematuria | numerous leukocytes and bacteria, WBC casts or bacterial casts | |
Chronic Pyelonephritis | increased urinary frequency, burning sensation while urinating and lower back pain | severe proteinuria and hematuria, and decreased renal concentration | numerous leukocytes and bacteria, WBC casts or bacterial casts, a variety of granular casts, waxy casts, and broad casts | |
Acute Interstitial Nephritis (AIN) | edema, fever, skin rashes | oliguria | hematuria, possibly macroscopic mild to moderate proteinuria, decreased renal concentrating ability, possible decrease of glomerular filtration rate | numerous WBCs, and WBC casts without the presence of bacteria |
Renal Failure | edema, and azotemia | oliguria | marked decrease in glomerular filtration (less than 25 mL/min); steadily risin BUN and creatinine values; electrolyte imbalance; isothenuric urine; proteinuria and renal glycosuria | abundant granular casts, waxy casts, and broad casts; either RTE cells and casts, RBCs, WBC casts or urothelial cells |
Renal Lithiasis | severe pain radiating from the lower back to the legs while urinating, urinary obstruction | microscopic hematuria | crystals |
Symptoms usually occur in children and young adults following respiratory infections caused by certain strains of group A streptococcus that contain M protein in the cell wall.
They form immune complexes with their corresponding circulating antibodies and become deposited on the glomerular membranes.
Demonstration of an elevated serum antistreptolysin O (ASO) titer or anti–group A streptococcal enzyme tests provide evidence that the disease is of streptococcal origin.
It does not produce permanent damage after treatment.
However, microscopic hematuria lasts until the membrane damage has been repaired.
Symptoms are initiated by deposition of immune complexes in the glomerulus from glomerulonephritis or an immune systemic disorder.
Macrophages migrate to the capillary walls and damage them, releasing cells and plasma into Bowman’s space and producing crescentic formations containing macrophages, fibroblasts and polymerized fibrin, causing permanent damage to the capillary tufts eventually leading to renal failure.
After viral respiratory infections, antiglomerular basement membrane antibodies are formed and attach to the basement membrane, causing capillary destruction.
Antineutrophilic cytoplasmic antibody (ANCA) bind to the neutrophils located in the vascular walls, causing granuloma formation.
It is a disease occurring primarily in children following upper respiratory infections.
Complete recovery with normal renal function is seen in more than 50% of patients while others progress to a more serious form of glomerulonephritis and renal failure.
It is characterized by pronounced thickening of the glomerular basement membrane resulting from the deposition of immunoglobulin G immune complexes.
It is associated with disorders such as systemic lupus erythematosus, Sjögren syndrome, secondary syphilis, hepatitis B, gold and mercury treatments, malignancy and even disorders of unknown origin.
It may be of two types which alters the cellularity of the glomerulus and peripheral capillaries.
Type 1 displays increased cellularity in the subendothelial cells of the mesangium (interstitial area of Bowman’s capsule), causing thickening of the capillary walls and progressing to nephrotic syndrome.
Type 2 displays extremely dense deposits in the glomerular basement membrane and progresses to chronic glomerulonephritis.
Many of the patients are children, and the disease has a poor prognosis.
It is characterized by IgA deposits in the glomerular membrane caused by increased levels in the serum as a result of mucosal infections.
The disorder is most frequently seen in children and young adults.
A patient with the disorder may remain essentially asymptomatic for 20 years or more with periodic recurrences of macroscopic hematuria; however, there is a gradual progression to chronic glomerulonephritis and end-stage renal disease.
It is usually a progression of glomerular disorders in which the permeability of the glomerular membrane is increased due to damage and changes in the electrical charges in the basal lamina and podocytes, producing a less tightly connected barrier.
This makes high-molecular-weight proteins and lipids that are normally filtered enter the urine, specifically albumin.
Albumin is depleted from the circulation, stimulating the increased production of lipids by the liver and lowering the oncotic pressure in the capillaries.
It causes fluid loss into the interstitial spaces and sodium retention, resulting in edema.
Depletion of immunoglobulins and coagulation factors places patients at an increased risk of infection and coagulation disorders.
Acute onset of the disorder can occur in instances of circulatory disruption, producing systemic shock that decrease the pressure and flow of blood to the kidney and progressing to tubular and glomerular damage that causes chronic renal failure.
Though there is little cellular change in the glomerulus, the podocytes appear to be less fitted, hampering filtration of protein.
Although the etiology is unknown at this time, allergic reactions, recent immunization, and possession of the human leukocyte antigen-B12 (HLA-B12) antigen have been associated, and it usually affects children.
The disorder responds well to corticosteroids, and prognosis is generally good, with frequent complete remissions.
It affects only certain numbers and areas of glomeruli, and the others remain normal.
Immune deposits are a frequent finding and can be seen in undamaged glomeruli.
It is often seen in association with abuse of heroin and analgesics and with AIDS.
It is a sex-linked or autosomal inherited disorder affecting the glomerular basement membrane.
Males are frequently more severely affected than females, and it progresses from the age of six during respiratory infections.
The glomerular basement membrane has a lamellated appearance with areas of thinning but there are no glomerular antibodies.
It is the most common cause of end-stage renal disease.
It involves damage to the glomerular membrane from glomerular membrane thickening, increased proliferation of mesangial cells and increased deposition of cellular and noncellular material within the glomerular matrix.
This is believed to be associated with deposition of glycosylated proteins resulting from poorly controlled blood glucose levels.
The vascular structure of the glomerulus also develops sclerosis.
This is caused by decreased blood flow leading to insufficient oxygen (ischemia), by the presence of toxic substances in the urinary filtrate, or by disorders such as shock, trauma and surgery.
Examples of toxic substances include aminoglycoside antibiotics, amphotericin B, cyclosporine, radiographic dye, organic solvents such as ethylene glycol, heavy metals, and toxic mushrooms.
Examples of conditions that may cause shock are cardiac failures, sepsis involving toxogenic bacteria, anaphylaxis, massive hemorrhage, and contact with high-voltage electricity.
Correction of the ischemia and removal of toxic substances followed by effective management of the accompanying symptoms of acute renal failure frequently result in a complete recovery.
It refers to a generalized failure of tubular reabsorption in the proximal convoluted tubule.
Therefore, substances most noticeably affected include glucose, amino acids, phosphorous, sodium, potassium, bicarbonate, and water.
Tubular reabsorption may be affected by dysfunction of the transport of filtered substances across the tubular membranes, disruption of cellular energy needed for transport or changes in the tubular membrane permeability.
It may be inherited or acquired through exposure to toxic agents such as heavy metals, outdated tetracycline or through complications of multiple myeloma and renal transplant.
It refers to the inability of the renal tubules to respond to ADH, leading to excessive excretion of urine.
It can be inherited as a sexlinked recessive gene, accquired from medications including lithium and amphotericin B, or a complication of polycystic kidney disease and sickle cell anemia.
This occurs when the maximal tubular reabsorption capacity (Tm) for glucose is reached and it can no longer be removed from the urine.
The disorder is inherited as an autosomal recessive trait, and in this case, either the number of glucose transporters in the tubules is decreased or the affinity of the transporters for glucose is decreased.
Infection may involve the lower urinary tract (urethra and bladder) or the upper urinary tract (renal pelvis, tubules, and interstitium).
Most frequently encountered is infection of the bladder (cystitis), which if untreated can progress to a more serious upper UTI.
Cystitis is seen more often in women and children who present with symptoms of urinary frequency and burning.
It refers to the infection of the upper urinary tract, including both the tubules and interstitium.
Acute pyelonephritis most frequently occurs as a result of ascending movement of bacteria from a lower UTI into the renal tubules and interstitium.
The ascending movement of bacteria from the bladder is enhanced with conditions that interfere with the downward flow of urine such as renal calculi, pregnancy and reflux of urine from the bladder back into the ureters (visicoureteral reflux).
A relatively high correlation between acute pylonephritis and bacteremia has been demonstrated, suggesting the need to perform blood cultures in addition to urine cultures.
With appropriate antibiotic therapy and removal of any underlying conditions, acute pyelonephritis can be resolved without permanent damage to the tubules.
It is a progression that results in permanent damage to the renal tubules and possible progression to chronic renal failure.
The most frequent cause is congenital urinary structural defects producing a reflux nephropathy that affects the emptying of the collecting ducts.
It is often diagnosed in children and may not be suspected until tubular damage has become advanced.
It refers to the inflammation of the renal interstitium followed by inflammation of the renal tubules.
It is primarily associated with an allergic reaction to medications that occurs within the renal interstitium, possibly caused by binding of the medication to the interstitial protein.
Symptoms tend to develop approximately 2 weeks following administration of medication.
Medications commonly associated with AIN include penicillin, methicillin, ampicillin, cephalosporins, sulfonamides, NSAIDs, and thiazide diuretics.
Discontinuation of the offending medication, administration of steroids to control the inflammation and supportive renal dialysis frequently results in a return to normal renal function.
It exists in both acute and chronic forms and may be a gradual progression from the original disorder to chronic renal failure or end-stage renal disease.
Acute renal failure (ARF), in contrast to chronic renal failure, exhibits a sudden loss of renal function and is frequently reversible.
Primary causes of ARF include a sudden decrease in blood flow to the kidney (prerenal), acute glomerular and tubular disease (renal), and renal calculi or tumor obstructions (postrenal).
The presence of RTE cells and casts suggests ATN of prerenal origin; RBCs indicate glomerular injury; WBC casts with or without bacteria indicate interstitial infection or inflammation of renal origin; and postrenal obstruction may show normal and abnormal appearing urothelial cells possibly associated with malignancy.
It refers to the formation of renal calculi of various sizes that may cause obstruction to urinary flow.
Conditions favoring the formation of renal calculi are similar to those favoring formation of urinary crystals, including pH, chemical concentration, and urinary stasis.
Analysis of the chemical composition of renal calculi plays an important role in patient management.
Analysis can be performed chemically, but examination using x-ray crystallography provides a more comprehensive analysis.
Approximately 75% of the renal calculi are composed of calcium oxalate or phosphate.
Magnesium ammonium phosphate (stuvite), uric acid, and cystine are the other primary calculi constituents.
Uric acid calculi may be associated with increased intake of foods with high purine content, so the urine pH is acidic.
Most cystine calculi are seen in conjunction with hereditary disorders of cystine metabolism.
Calcium calculi are frequently associated with metabolic calcium and phosphate disorders and occasionally diet.
Magnesium ammonium phosphate calculi are frequently accompanied by urinary infections involving urea-splitting bacteria, so the urine pH is often higher than 7.0.
It is addressed by using lithotripsy, a procedure that breaks the stones using high-energy shock waves, or surgical removal.
Patient management techniques include maintaining the urine at a pH incompatible with crystallization of the particular chemicals, maintaining adequate hydration to lower chemical concentration, and suggesting possible dietary restrictions.
Disease | Symptoms | Physical Findings | Chemical Findings | Microscopic Findings |
|---|---|---|---|---|
Acute Poststreptococcal Glomerulonephritis (AGN) | sudden onset of fever, edema around the eyes, fatigue and hypertension | oliguria | hematuria, proteinuria increased BUN | RBC casts, dysmorphic RBCs, hyaline and granular casts and WBCs |
Rapidly Progressive (Crescentic) Glomerulonephritis (RPGN) | progression of AGN, renal failure | oliguria | hematuria, proteinuria, increased BUN, fibrin degradation products, cryoglobulins and IgA immune complexes | RBC casts, dysmorphic RBCs, hyaline and granular casts and WBCs |
Goodpasture syndrome | hemoptysis (spitting out blood from lungs) and dyspnea (shortness of breath) | hematuria, proteinuria, presence of antiglomerular basement membrane antibodies in blood serum | RBC casts | |
Wegener’s Granulomatosis | pulmonary symptoms, granulomas in the small blood vessels of the kidney and respiratory system | hematuria, proteinuria, presence of antineutrophilic cytoplasmic antibody (ANCA) in the blood serum, elevated serum creatinine and BUN | RBC casts | |
Henoch-Schönlein Pupura | raised red patches on the skin, blood in the sputum and stools, progression to glomerulonephritis and renal failure | mild to heavy proteinuria and hematuria | RBC casts | |
Membranous Glomerulonephritis | nephrotic syndrome symptoms and thrombosis, slow progression with possible remission | microscopic hematuria and proteinuria | ||
Membranoproliferative Glomerulonephritis | autoimmune disorders, infections and malignancies. | hematuria and proteinuria, decreased blood serum complement levels | ||
Immunogloblin A Nephropathy/Berger Disease | progression of glomerular disorders, fatigue, anemia, hypertension and edema | oliguria | macroscopic hematuria, proteinuria, glucosuria, markedly decreased glomerular filtration rate, increased BUN and creatinine, electrolyte imbalance, increased serum IgA levels | many varieties of casts including broad casts |
Nephrotic Syndrome | pronounced edema | massive proteinuria (greater than 3.5 g/d), microscopic hematuria, low serum albumin and high serum lipids | urinary fat droplets, oval fat bodies, RTE cells; and epithelial, fatty, and waxy casts | |
Minimal Change Disease/Lipid Nephropathy | edema | heavy proteinuria, transient hematuria | ||
Focal Segmental Glomerulosclerosis (FSGS) | edema | immunoglobulins M and C3, moderate to heavy proteinuria and microscopic hematuria | ||
Alport Syndrome | abnormalities in hearing and vision from the age of six, renal insufficiency in later life, progression to nephrotic syndrome and end-stage renal disease | macroscopic and microscopic hematuria | ||
Diabetic Nephropathy/Kimmelstiel-Wilson Disease | ||||
Acute Tubular Necrosis (ATN) | mild proteinuria and microscopic hematuria | RTE cells and RTE cell casts containing tubular fragments consisting of three or more cells; hyaline casts, granular casts, waxy casts and broad casts | ||
Fanconi Syndrome | glycosuria and possible mild proteinuria | |||
Nephrogenic Diabetes Insipidus | low specific gravity and pale yellow color | possible false-negative results for chemical test | ||
Renal Glycosuria | ||||
Urinary Tract Infection (UTI) | mild proteinuria and hematuria, increased pH | numerous WBCs and bacteria | ||
Acute Pyelonephritis | increased urinary frequency, burning sensation while urinating and lower back pain | mild proteinuria and hematuria | numerous leukocytes and bacteria, WBC casts or bacterial casts | |
Chronic Pyelonephritis | increased urinary frequency, burning sensation while urinating and lower back pain | severe proteinuria and hematuria, and decreased renal concentration | numerous leukocytes and bacteria, WBC casts or bacterial casts, a variety of granular casts, waxy casts, and broad casts | |
Acute Interstitial Nephritis (AIN) | edema, fever, skin rashes | oliguria | hematuria, possibly macroscopic mild to moderate proteinuria, decreased renal concentrating ability, possible decrease of glomerular filtration rate | numerous WBCs, and WBC casts without the presence of bacteria |
Renal Failure | edema, and azotemia | oliguria | marked decrease in glomerular filtration (less than 25 mL/min); steadily risin BUN and creatinine values; electrolyte imbalance; isothenuric urine; proteinuria and renal glycosuria | abundant granular casts, waxy casts, and broad casts; either RTE cells and casts, RBCs, WBC casts or urothelial cells |
Renal Lithiasis | severe pain radiating from the lower back to the legs while urinating, urinary obstruction | microscopic hematuria | crystals |
