Nephrology/Urology Week #1 Review - In progress

Clear cell most common subtype

Renal Cell Carcinoma

Cigarette smoking is most important environmental risk factor

Renal Cell Carcinoma

Associated with hypertension, obesity, dialysis, and male sex

Renal Cell Carcinoma

Classic triad of hematuria, flank or abdominal pain, & palpable abdominal or flank mass

Renal Cell Carcinoma

Possible paraneoplastic signs/symptoms include hypertension, hypercalcemia, anemia, hepatic dysfunction, fever, and/or cachexia

Renal Cell Carcinoma

Acute onset left-sided varicocele

Renal Cell Carcinoma

Abdominal CT scan with and without contrast is diagnostic study of choice

Renal Cell Carcinoma

Lung is most common site of metastasis (CT chest)

Renal Cell Carcinoma

Managed with partial vs. radical nephrectomy for stages 1-3

Renal Cell Carcinoma

Managed with radical nephrectomy + chemotherapy/radiation in stage 4 disease

Renal Cell Carcinoma

Also known as renovascular hypertension

Renal Artery Stenosis

Most common cause of secondary hypertension

Renal Artery Stenosis

Atherosclerosis is most common etiology overall (especially in elderly)

Renal Artery Stenosis

New onset or resistant HTN in women < 50 years

Fibromuscular dysplasia

Decreased renal blood flow leads to activation of the renin angiotensin aldosterone system (RAAS)

Renal Artery Stenosis

Suspect if onset of hypertension < 30 or onset of severe hypertension > 55, especially with headache

Renal Artery Stenosis

Suspect if abdominal bruit present on physical exam

Renal Artery Stenosis

Suspect if AKI develops after initiation of ACE inhibitor

Renal Artery Stenosis

Suspect if hypertension resistant to ≥ 3 drugs

Renal Artery Stenosis

Noninvasive diagnostic imaging such as CT angiography w/ contrast or renal ultrasound w/ doppler used first-line

Renal Artery Stenosis

Renal angiography is definitive diagnostic test, but is reserved for patients in which there is high suspicion and anticipated benefit from intervention like revasularization

Renal Artery Stenosis

"String of pearls" appearance in renal arteries on angiography

Fibromuscular Dysplasia

Medical management with ACE-I/ARB is first-line

Renal Artery Stenosis

Avoid ACE-I/ARBs in patients with bilateral stenosis or a solitary kidney

Renal Artery Stenosis

Definitive management via angioplasty w/ or w/o stenting in severe/refractory cases

Renal Artery Stenosis

Kidney disease characterized by proteinuria (> 3.5 grams/24 hours, mostly albuminuria), hypoalbuminemia, edema, hyperlipidemia, & thromboembolic disease

Nephrotic Syndrome

Most common cause of Nephrotic syndrome in children

Minimal change disease

Hypercoagulable state due to loss of anticoagulant proteins

Nephrotic Syndrome

Oval fat bodies on urinalysis

Nephrotic Syndrome

General management with sodium & protein restriction, ACE-I/ARBs, BP control, treatment of hyperlipidemia, & anticoagulation

Nephrotic Syndrome

Renal biopsy used for definitive diagnosis

Nephrotic syndrome, Nephritic syndrome

Associated with viral infections, SLE, malignancies, & medications (NSAIDs)

Minimal change disease, Membranous nephropathy

May be secondary to allergies (i.e. insect stings)

Minimal change disease

No cellular changes on light microscopy and podocyte funsion on EM

Minimal change disease

Treat with corticosteroids

Minimal change disease

Most common cause of nephrotic syndrome in non-diabetic adults

Membranous nephropathy

Managed with immunosuppression in moderate-to-high-risk patients

Membranous nephropathy

Managed with glucocorticoids +/- tacrolimus

Focal segmental glomerulosclerosis (FSGS)

Secondary causes include obesity, heroin, and HIV

Focal segmental glomerulosclerosis (FSGS)

Most common overall cause of Nephrotic syndrome & CKD in the US

Diabetic nephropathy

Management includes SLGT-2 inhibitor if Type 2

Diabetic nephropathy

Usually diagnosed without a renal biopsy

Diabetic nephropathy, Post-streptococcal glomerulonephritis

Immunologic inflammation of the glomeruli

Nephritic syndrome

Hypertension, hematuria, azotemia, & proteinuria (edema)

Nephritic syndrome

Etiologies include IgA nephropathy, post-infectious glomerulonephritis, membranoproliferative glomerulonephritis, & rapidly progressive glomerulonephritis

Nephritic syndrome

Hematuria hallmark (e.g. cola, dark-colored, or tea-colored urine)

Nephritic syndrome

Most common cause of primary glomerulonephritis

IgA nephropathy

History of URI/GI infection within 2 weeks

IgA nephropathy

Occurs 2-3 weeks after streptococcal infection

Post-Streptococcal Glomerulonephritis

Low serum complement (C3) + elevated ASO

Post-Streptococcal Glomerulonephritis

Manage with diuretics for fluid overload & antibiotics if active infection still present

Post-Streptococcal Glomerulonephritis

Histologic lesions, not specific disease entity

Focal segmental glomerulonephritis (FSGN), Membranoproliferative glomerulonephritis (MPGN)

Thickened basement membrane is hallmark

Membranoproliferative glomerulonephritis (MPGN)

Anti-dsDNA antibodies

Lupus Nephritis

Rapidly progressive glomerulonephritis + alveolar hemorrhage (hemoptysis)

Goodpasture's Syndrome

Antiglomerular basement membrane (GBM) antibodies against kidney and lungs

Goodpasture's Syndrome

Treat with corticosteroids & cyclophosphamide + plasmapheresis

Goodpasture's Syndrome

C-ANCA positivity

Granulomatosis with polyangiitis (GPA)

P-ANCA positivity

Microscopic polyangiitis (MPA), Eosinophilic granulomatosis with polyangiitis (EGPA)

Upper RT involvement (hemoptysis) & lower RT involvement (nasal ulcers) + nephritis

Granulomatosis with polyangiitis (GPA)

Nephritis with mild respiratory symptoms

Microscopic polyangiitis (MPA)

Nephritis with asthma, allergic rhinitis, & peripheral eosinophilia

Eosinophilic granulomatosis with polyangiitis (EGPA)

Managed with glucocorticoids + Rituximab or Cyclophosphamide

Granulomatosis with polyangiitis (GPA), Microscopic polyangiitis (MPA)

Abrupt decrease in kidney function, resulting in the retention of urea and other nitrogenous waste products

Acute kidney injury (AKI)

Etiology may be prerenal, postrenal, or intrarenal

Acute kidney injury (AKI)

< 400/500 ml of urine produced in 24 hours

Oliguria

< 100 ml of urine produced in 24 hours

Anuria

Decreased renal perfusion with nephrons still structurally intact

Prerenal azotemia

May be due to low cardiac output (i.e. CHF), change in vascular resistance (i.e. ACE-I/ARB, NSAIDs), or volume depletion (i.e. hemorrhage, dehydration)

Prerenal azotemia

BUN: creatinine ratio > 20:1

Prerenal azotemia

FENa < 1%

Prerenal azotemia

Mainstay of management is volume repletion

Prerenal azotemia

GFR < 60 or evidence of kidney damage for ≥ 3 months

Chronic kidney disease

Kidney damage with normal GFR ≥ 90

Stage 1 CKD

GFR 60-89

Stage 2 CKD

GFR 45-59

Stage 3a CKD

GFR 30-44

Stage 3b CKD

GFR 15-29

Stage 4 CKD

GFR < 15

Stage 5 CKD

Uremia requiring dialysis and/or transplant

End Stage Renal Disease (ESRD)

Diabetes mellitus is #1 cause and hypertension is #2 cause

CKD, ESRD

Waxy casts

Chronic kidney disease (CKD)

RBC casts

Nephritic Syndrome

Muddy brown casts

Acute tubular necrosis (ATN)

Fatty casts

Nephrotic Syndrome

Bilateral small, echogenic kidneys on renal ultrasound in advanced disease

Chronic kidney disease (CKD)

Hypertension is most common complication

Chronic kidney disease (CKD)

Managed with ACE/ARB + loop diuretic, salt restriction, & exercise

Hypertension in CKD

Normochromic normocytic anemia due to decreased EPO production & increased Hepcidin

Anemia of CKD

Manage with iron supplementation as indicated with EPO-stimulating agents with Hgb < 10

Anemia of CKD

Managed in sequence with ACE-I/ARB + SGLT2i + NS-MRA

Diabetic kidney disease

eGFR decline > 5 mL/min/year

Progressive CKD

Autosomal dominant mutation in PKD1 gene

Autosomal dominant polycystic kidney disease (ADPKD)

Extrarenal manifestations include liver cysts, cerebral aneurysms, and mitral valve prolapse

Autosomal dominant polycystic kidney disease (ADPKD)

Preserved renal function until 4th decade of life typically w/ average age of diagnosis 25-45 years old

Autosomal dominant polycystic kidney disease (ADPKD)

Multiple renal cysts of varying sizes bilaterally on renal ultrasound

Autosomal dominant polycystic kidney disease (ADPKD)

Family history of renal disease, dialysis, renal transplant, cerebral aneurysms, sudden unexplained death, etc.

Autosomal dominant polycystic kidney disease (ADPKD)

Management includes BP control with ACE-I/ARBs, increased fluid intake, and restriction of dietary sodium & protein

Autosomal dominant polycystic kidney disease (ADPKD)

Autosomal recessive mutation of PHKD1 gene

Autosomal recessive polycystic kidney disease (ARPKD)

Fibrocystic changes in kidneys + congenital hepatic fibrosis

Autosomal recessive polycystic kidney disease (ARPKD)