W3 Renal Disease, Glomeruloneph, Nephrotic/phritic, Diabetic, Hydronephrosis, Polycystic Etc Flashcards

1
Q

26-year-old man who presents with hematuria, periorbital edema, and jaundice.

He has a medical history of opioid use disorder with prior hospitalizations for a heroin overdose.

He is on Suboxone but is non-adherent.

His blood pressure is 162/102 mmHg. Physical examination is significant for scleral icterus, hepatomegaly, and palpable purpura.

Serology shows decreased C3 and C4 levels and elevated anti-hepatitis C antibodies.

Urinalysis demonstrates dysmorphic red blood cells and red blood cell casts

A

Glomerulonephritis

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2
Q

Acute glomerulonephritis is an inflammation of glomeruli causing _____ and _____ leakage into the urine, typically caused by an ______

Two types and their characteristics

A

Acute glomerulonephritis is an inflammation of glomeruli causing protein and RBC leakage into the urine, typically caused by an immune response

Two types based on 24-hour urine protein

Nephritic syndrome:
hematuria
—HTN
moderate proteinuria 1-3.5 g/day

Nephrotic syndrome:
—edema
severe proteinuria > 3.5 g/day

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3
Q

Classic presentation: edema + HTN + hematuria + RBC Casts/dysmorphic RBCs + proteinuria 1-3.5 g/day + azotemia

A

Nephritic syndrome:

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4
Q

Etiologies of nephritic syndrome — 5
Which is the most common?

A
  1. Postinfectious - Group A strep (skin or throat) - 10-14 days
  2. IgA Nephropathy (Berger disease) - most common cause of acute glomerulonephritis worldwide
  3. Alport’s Syndrome
  4. Membranoproliferative glomerulonephritis (MPGN) - due to SLE, viral hepatitis
  5. Rapidly progressive glomerulonephritis - crescent formation on biopsy due to fibrin and plasma protein deposition
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5
Q

a 10 y/o is brought to the clinic with her mother for dark urine. The mother mentions that the child was complaining of sore throat and cough/cold symptoms two weeks ago. The urine shows gross hematuria without nitrites or leukocytes.

What is the diagnosis?
Which labs?

A

Nephritic syndrome
Postinfectious - Group A strep (skin or throat) - 10-14 days after infection - diagnosed with ASO titers and low serum complement -

+ASO titers
Serum C3 C4 can be low (complement)

treatment is supportive + antibiotics

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6
Q

a 33-year-old man who comes to the ED because of blood in his urine for 2 days.

He has also been feeling unwell, with a sore throat, running nose, cough, and fever.

Medical history includes three episodes of hematuria in the past that have spontaneously resolved. His temperature is 98.9°F; pulse is 82/min; respirations are 18/min, and blood pressure is 145/90 mm Hg. PE is normal.

Urinalysis shows moderate numbers of erythrocytes, a few leukocytes, red cell casts, and a large amount of protein. No bacteria are cultured. A renal biopsy demonstrates large dark mesangial deposits.

A

Nephritic syndrome
2. IgA Nephropathy (Berger disease)
—most common cause of acute glomerulonephritis worldwide

—Gross hematuria and flank pain in a person with acute URI
—Often affects young males within days (24-48 hours) after URI or GI infection
—Caused by IgA immune complexes which are the first line of defense in respiratory and GI secretions so infections cause an overproduction which then damages the kidneys
—Diagnosed by (+) IgA deposits in mesangium and with immunostaining

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7
Q

a 15-year-old boy who comes to the office because of malaise, anorexia, nausea, and decreased urination. His mother says that he is having problems hearing. Physical examination shows decreased hearing bilaterally with the

Rinne test and bilateral edema in the lower extremities. Urinalysis shows microscopic hematuria and proteinuria.

A peripheral blood smear reveals microcytic anemia.

A

Nephritic Syndrome: Alpert’s syndrome

—Presents as isolated persistent hematuria
—A genetic condition that occurs in children resulting in renal failure and hearing loss
Ophthalmologic exam reveals anterior lenticonus - anterior part of the lens has a conical shape
—DX - C3 and C4 Levels

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8
Q

a 26-year-old man who presents with hematuria, periorbital edema, and jaundice. He has a medical history of opioid use disorder with prior hospitalizations for a heroin overdose. He is on Suboxone but is non-adherent. His blood pressure is 162/102 mmHg. Physical examination is significant for scleral icterus, hepatomegaly, and palpable purpura. Serology shows decreased C3 and C4 levels and elevated anti-hepatitis C antibodies. Urinalysis demonstrates dysmorphic red blood cells and red blood cell casts.

A

Nephritic syndrome
4. Membranoproliferative glomerulonephritis (MPGN) - due to SLE, viral hepatitis

MPGN describes an injury to the glomerulus secondary to immune-complex deposition and/or a complement-mediated mechanism
Deposition of immune-complexes or complement proteins results in an inflammatory response that leads to glomerular injury
In response to this injury, the cell undergoes a number of changes such as mesangial proliferation, remodeling of the capillary wall, and development of a new basement membrane
MPGN can be idiopathic or result from a secondary condition, such as hepatitis C virus (HCV) infection

↓ serum C3 and C4 levels

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9
Q

a 27-year-old male presents to the clinic complaining of coughing up small amounts of blood daily for the past week. He denies smoking, sick contacts, or recent travel. Chest radiographs demonstrate interstitial pneumonia with patchy alveolar infiltrates suggestive of multiple bleeding sites. Urinalysis is positive for blood and protein. A positive result is returned for anti-glomerular basement membrane antibody (anti-GBM Ab)

A

Nephritic Syndrome

  1. Rapidly progressive glomerulonephritis - crescent formation on biopsy due to fibrin and plasma protein deposition

Goodpasture’s syndrome: (+) anti-GBM antibodies, dx linear IgG deposits, treat with high dose steroids, plasmapheresis + cyclophosphamide

Vasculitis - lack of immune deposits (+) ANCA antibodies
—Microscopic polyangiitis (+) P-ANCA
—Granulomatosis with polyangiitis (Wegener’s) (+) C-ANCA

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10
Q

❗️[must know]
Glomerulonephritis
UA will reveal what 3 things
GFR will be high or low?
What else do you see in 60-80% of cases which could indicate a recent infection of what?
C3 is increased or decreased?
What is the gold standard to determine exact diagnosis?

A

Urinalysis reveals
hematuria (>3 RBCs / high power field)
misshaped RBCs (RBC casts) due to their passage through the glomerulus, and
proteinuria (1-3.5 g/24 hours)

GFR low

—An anti-strepto-lysin-o titer is increased in 60-80% of cases and should be considered if there is a possibility of recent streptococcal infection

—run hepatitis serology

—Serum complement (C3) is often decreased

Renal biopsy is the GOLD STANDARD may be done to determine the exact diagnosis and severity of the disease

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11
Q

Glomerulonephritis treatment

A

Steroids and immunosuppressive drugs may be used to control the inflammatory response

—Dietary management: salt and fluid restriction
—Dialysis should be performed if symptomatic azotemia
ACEI/ARBs (enalapril or losartan) are renoprotective - blood pressure goal < 130/80

⭐️In poststreptococcal GN Nifedipine is used instead of ACEI (ACE may cause hyperkalemia) ⭐️

—IgA nephropathy - Glucocorticoids
—Rapidly progressive glomerulonephritis - immunosuppressive therapy
—Use medications to control hyperkalemia, pulmonary edema, peripheral edema, acidosis and hypertension

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12
Q

Diabetic nephropathy

Most common cause of ______
Hyperfiltration — increased ______ / ______ — progressive decline in ______

Tx: (5)

______ is pathognomonic**

A

Most common cause of ESRD
Hyperfiltration — increased proteinuria / albuminuria — progressive decline in GFR

Tx:
—Blood glucose
—BP control
—RAAS inhibitors (ACEI/ARB)
—monitor for hyperkalemia
—SGLT inhibitors (~gliflozin)

glomerulosclerosis (Kimmelstiel-Wilson nodules) is pathognomonic

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13
Q

48-year-old woman who presents to the emergency department due to severe back pain and difficulty urinating. Her symptoms began approximately 3 hours ago and is associated with pain in her left mid-back which she describes as 9/10 and sharp. The pain radiates to her left groin. On physical exam, there is left-sided costovertebral angle tenderness. A non-contrast computerized tomography (CT) scan of the abdomen demonstrates left-sided urolithiasis and hydronephrosis. She is started on a nonsteroidal anti-inflammatory drug (NSAID) and intravenous normal saline.

A

Hydronephrosis

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14
Q

Hydronephrosis — refers to ______ of the renal ______ and ______, usually caused by ______ of the free flow of urine from the kidney.

Causes include 4

Symptoms include ______ and ______

A

Hydronephrosis — refers to distension and dilation of the renal pelvis and calyces, usually caused by obstruction of the free flow of urine from the kidney.

Causes include
—a kidney stone
—an infection
vesicoureteral reflux
—an enlarged prostate
—a blood clot, or a tumor

Symptoms include difficulty urinating and
pain in the side, abdomen, or radiating to groin (testicles/labia)

In cases of hydroureteronephrosis, there is distention of both the ureter and the renal pelvis and calyces

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15
Q

Hydronephrosis diagnosis

A

—impaired kidney function = elevated urea and creatinine
—palpable abdominal mass/flank pain
—UA: elevated pH
—PVR = >100ml
U/S, then CT urogram, CT, MRI

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16
Q

Hydronephrosis treatment

A

—removal and drainage
—upper urinary tract obstruction: insertion of nephrostomy tube. If chronic ureteric stent or a pyeloplasty
—lower obstruction: urinary catheter or suprapubic catheter
—abx if infection (bactrim or nitro x3-4w

hydronephrosis w/ infection = urologic emergency

17
Q

Glomerulonephritis — pathophysiology

—inflammatory process
—cellular proliferation: excess of ______, ______, ______, This can occur in within the ______, or in the ______,
—proliferation in the bowman space causes the formation of ______, which can be rapidly progressive
—glomerular basement membrane ______, and appears on microscopy
—irreversible injury includes ______, or ______, this is the end result

A

—inflammatory
—cellular proliferation: excess of endothelial, mesangial, epithelial cells, This can occur in within the glomerular capillary tufts or in the Bowman space
—proliferation in the bowman space causes the formation of crescents which can be rapidly progressive
—glomerular basement membrane thickens and appears on microscopy
—irreversible injury includes hyalinisation or sclerosis this is the end result.

18
Q

Pediatric patient develops acute periorbital puffiness and facial swelling in the background of a post-streptococcal infection 3 weeks ago. Has dark, frothy, and scanty urine. BP is high

A

Acute glomerulonephritis

19
Q

Dark urine, specific gravity of >1.020 with RBCs
24-urine shows proteinuria

A

Glomerulonephritis

20
Q

Specific management for glomerulonephritis revolves around ______. Available options are:
—high dose ______.
—______.
—______.
—______.

You also have to treat the progression to ______.

A

Specific management for glomerulus revolves around immunosuppression. Available options are:
—high dose corticosteroids
rituxumab
—cyclophosphamide
—plasma exchange

You also have to treat the progression tochronic kidney disease

21
Q

❗️[must know]
Treatment for
Minimal change disease
Focal segmental glomerularsclerosis
Membranoproliferative GN

A

❗️[must know]
Minimal change disease:
Prednisone 1 mg/kg (4 to 16 weeks). If relapsing, immunosuppression with greater intensity or for longer durations are options.
—Cyclophosphamide and calcineurin inhibitors are effective options.

Focal segmental glomerulosclerosis:
—Treatment initially with ACE inhibitors/ARBs
and by controlling BP.
—Calcineurin inhibitors, plasma exchange, corticosteroids,
and rituximab are helpful treatment options.

Membranoproliferative GN:
—Treatment is done initially with ACE inhibitors/ARBs
and by controlling BP.
—Immunosuppression is useful if no underlying cause is
found. Work is currently ongoing to block or modify C3 activation.

22
Q

a 34-year-old male with hematuria and flank/abdominal pain. He denies any recent trauma. He reports a history of recurrent urinary tract infections, and his family history is significant for his mother who died of a “brain bleed” at age 42. Vital signs are significant for a blood pressure of 158/105 mmHg. On physical exam, there is a late systolic crescendo murmur with a midsystolic click and tenderness upon palpation of the abdominal flanks. An ultrasound of the abdomen shows bilateral anechoic renal cysts with posterior enhancement.

A

Polycystic kidney disease

23
Q

______ is characterized by the growth of numerous cyst in the kidneys. The cysts are made of ______ from the ______. The cysts replace the ______ of the kidneys and reduce function leading to kidney failure

Polycystic kidney disease presents frequently with ______ with ______ or ______

A ______ is present in up to 75% of cases. Whenever patients present with resistant ______ and a ______, the diagnosis of ADPKD should be entertained.”

10% will complain of the worst _______ ever

A

Polycystic kidney disease is characterized by the growth of numerous cyst in the kidneys. The cysts are made of epithelial cells from the renal tubules. The cysts replace the mass of the kidneys and reduce function leading to kidney failure

Polycystic kidney disease presents frequently with abdominal or flank pain with microscopic or gross hematuria.

A family history is present in up to 75% of cases. Whenever patients present with resistant hypertension and a palpable abdominal mass, the diagnosis of ADPKD should be entertained.”

10% will complain of the worst headache ever

24
Q

How do you diagnose polycystic kidney disease? 2

A

ultrasound
Shows the fluid filled cysts

Test family members as well.

Genetic studies for PKD1 and PKD2

25
Q

What are the treatments for ADPKD

A

—no cure, treatment is supportive
control hypertension with an ACEI or ARB

26
Q

Large, echogenic kidneys with poor corticomedullary differentiation points to?

Patients will high risk features may be treated with what?

A

Polycystic kidney disease

Tolvaptan — vasopressin receptor antagonist

27
Q

a 69-year-old man with a 55-pack-year smoking history, diabetes type II, and hyperlipidemia presents to his primary care clinic for an annual exam. He has no complaints. He reports that his blood glucose has been under tight control and that he has not smoked a cigarette for the past 5 months. Vital signs are HR 69 bpm, BP 180/100 mmHg, RR 12/min, and O2 saturation 99% on room air.

Physical examination is notable for bruits bilaterally just lateral of midline near his umbilicus. You initiate an anti-hypertensive medication, but his blood pressure continues to be suboptimal. Creatinine is 3.5.

What is the diagnosis is?
Which anti-HTN meds should be avoided?
Which diuretic should be avoided?
What would you hear on auscultation?

A

Renal vascular disease
Renal artery stenosis

Avoid ACE/ARBs because they can induce or worsen renal insufficiency

Avoid thiazide diuretics too

Renal bruits on auscultation

28
Q

Gold standard test to diagnose renal vascular disease?
With that said, what is the first test?
And the next best test?

A

Renal arteriography

Although doppler ultrasound is often the initial imaging study following by CT angiography

29
Q

How do you treat renal vascular disease?

A

—stenting of arteries
—percutaneous trans liminal angioplasty (PTA) plus stent placement
— if kidney is completely infarcted, removal