NP31 Nephrology

Hypertension/Cystic Diseases of the Kidney

Essential Med Notes 2015

Hypertensive Nephrosclerosis
Table 12. Chronic vs. Malignant Nephrosclerosis
Histology

Chronic Nephrosclerosis

Malignant Nephrosclerosis

Slow vascular sclerosis with ischemic changes

affecting intralobular and afferent arterioles

Fibrinoid necrosis of arterioles, disruption of vascular

endothelium

Clinical Picture African American, underlying CKD, chronic

hypertensive disease

Acute elevation in BP (dBP >120 mmHg)

HTN encephalopathy

Urinalysis

Mild proteinuria, normal urine sediment

Therapy

Blood pressure control, (target <140/90) with frequent Lower dBP to 100-110 mmHg within 6-24 h
follow-up
More aggressive treatment can cause ischemic event
Identify and treat underlying cause of HTN

Proteinuria and hematuria (RBC casts)

Prognosis

Can progress to renal failure despite patient adherence

Lower survival if renal insufficiency develops

Renovascular Hypertension
see Vascular Diseases of the Kidney, NP17

Renal Parenchymal Hypertension

HTN secondary to GN, AIN, diabetic nephropathy, or any other chronic renal disease
mechanism of HTN not fully understood but may include
excess RAAS activation due to inflammation and fibrosis in multiple small intra-renal vessels
production of unknown vasopressors, lack of production of unknown vasodilators, or lack of
clearance of endogenous vasopressor
ineffective sodium excretion with fluid overload
Investigations
as well as investigations for renovascular HTN, additional tests may include
24 h urinary estimations of Cr clearance and protein excretion
imaging (U/S, CT)
serology for collagen-vascular disease
renal biopsy
Treatment
most chronic renal disease is irreversible, but treatment of HTN can slow the progression of
renal insufficiency
control ECF volume: Na+ restriction (88 mEq/d intake), diuretic, dialysis with end-stage disease
ACEI or ARB may provide added benefit (monitor K+ and Cr) if there is significant proteinuria
(>300 mg/d)

Cystic Diseases of the Kidney

characterized by epithelium-lined cavities filled with fluid or semisolid debris within the kidneys
includes: simple cysts (present in 50% of population over 50), medullary cystic kidney,
medullary sponge kidney, polycystic kidney disease (autosomal dominant and recessive), and
acquired cystic kidney disease (in chronic hemodialysis patients)

Adult Polycystic Kidney Disease

autosomal dominant; at least 2 genes: PKD1 (chr 16p) and PKD2 (chr 4q)
PKD1 (1:400), PKD2 (1:1,000) accounts for about 10% of cases of renal failure
patients generally heterozygous for mutant polycystin gene but accumlate a series of second
somatic hits precipitating the condition
PKD1 encodes a protein that is responsible for cell-cell and cell-matrix interaction and sensing
fluid flow by associating with cilia
PKD2 encodes a protein that is a Ca2+ permeable nonselective cation channel that associates
with cilia and is thought to control intracellular Ca2+ in response to flow
defect leads to abnormal proliferation and apoptosis of tubular epithelial cells leading to cyst growth
extrarenal manifestations: most common; multiple asymptomatic hepatic cysts (33%), cerebral
aneurysm (10%), diverticulosis, and mitral valve prolapse (25%)
polycystic liver disease rarely causes liver failure
less common: cysts in pancreas, spleen, thyroid, ovary, seminal vesicles, and aorta

Hypercalcemia complicates many

cancers and can cause multiple kinds of
renal disorders (renal vasoconstriction
with reduced OTR, salt-wasting with
volume depletion, risk of calcium kidney
stones)