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Pathology
Renal agenesis
Horseshoe kidney
Potter sequence
Hyperphosphatemia
Hypophosphatemia
Hypernatremia
Hyponatremia
Hypermagnesemia
Hypomagnesemia
Hyperkalemia
Hypokalemia
Hypercalcemia
Hypocalcemia
Renal tubular acidosis
Minimal change disease
Diabetic nephropathy
Focal segmental glomerulosclerosis (NORD)
Amyloidosis
Membranous nephropathy
Lupus nephritis
Membranoproliferative glomerulonephritis
Poststreptococcal glomerulonephritis
Goodpasture syndrome
Rapidly progressive glomerulonephritis
IgA nephropathy (NORD)
Lupus nephritis
Alport syndrome
Kidney stones
Hydronephrosis
Acute pyelonephritis
Chronic pyelonephritis
Prerenal azotemia
Renal azotemia
Acute tubular necrosis
Postrenal azotemia
Renal papillary necrosis
Renal cortical necrosis
Chronic kidney disease
Polycystic kidney disease
Multicystic dysplastic kidney
Medullary cystic kidney disease
Medullary sponge kidney
Renal artery stenosis
Renal cell carcinoma
Angiomyolipoma
Nephroblastoma (Wilms tumor)
WAGR syndrome
Beckwith-Wiedemann syndrome
Posterior urethral valves
Hypospadias and epispadias
Vesicoureteral reflux
Bladder exstrophy
Urinary incontinence
Neurogenic bladder
Lower urinary tract infection
Transitional cell carcinoma
Non-urothelial bladder cancers
Congenital renal disorders: Pathology review
Renal tubular defects: Pathology review
Renal tubular acidosis: Pathology review
Acid-base disturbances: Pathology review
Electrolyte disturbances: Pathology review
Renal failure: Pathology review
Nephrotic syndromes: Pathology review
Nephritic syndromes: Pathology review
Urinary incontinence: Pathology review
Urinary tract infections: Pathology review
Kidney stones: Pathology review
Renal and urinary tract masses: Pathology review
Nephritic syndromes: Pathology review
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On the nephrology ward, two people came in with the same symptoms: peripheral and periorbital edema, along with cola-colored urine, arterial hypertension and decreased urine output.
The first person is 10 year old Timmy who had a throat infection two weeks ago.
The second one is 45 year old Dorothy, who also presents with hemoptysis.
Lab tests show that both of them have increased creatinine and BUN.
On urinalysis, there’s hematuria and red blood cell casts in the urine.
A 24-hour protein collection was done and showed that both Timmy and Dorothy had proteinuria, but in both cases it was less than 3.5 grams per day.
Now, both Timmy and Dorothy have nephritic syndrome.
Nephritic syndrome is typically caused by inflammation that damages the glomerular basement membrane, leading to hematuria and red blood cell casts in the urine.
Eventually, this damage can lead to renal failure, where the individual can present with oliguria, arterial hypertension, due to sodium retention, and peripheral and periorbital edema.
Lab tests show high levels of BUN and creatinine and on urinalysis, there’s hematuria, proteinuria and RBC casts in the urine.
A 24-hour protein collection is necessary to quantify how many proteins are lost through urine.
Now, nephritic syndrome can be differentiated from nephrotic syndrome because the proteinuria is generally under 3.5 grams per day, or within the “subnephrotic range”.
In severe cases though, proteinuria can reach over 3.5 grams per day.
In order to determine the cause, a careful history and a kidney biopsy can help diagnose the particular disease.
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