Renal Diseases

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Acute Renal Failure
Prerenal azotemia
Renal azotemia
Postrenal azotemia

Chronic Renal Failure
General/causes
Clinical manifesations

Acute Renal Failure

General
-rapid deterioration in renal function which results in retention in nitrogenous waste products (azotemia)
-nitrogenous waste products (azotemia) act like toxins and are by-products of protein metabolism and amin acids
ex. urea, guanidine compounds, urates, aliphatic amines along with other peptides of aromatic amino acid metabolism
-causes of acute renal failure vary but the progression may be generalised
-oliguria phase usually last around 2 weeks
-diuretic phase with increased urine output (usually absent in nonoliguric renal failure)
-then improvement in urinary function within several weeks upto one year

PRERENAL AZOTEMIA
causes
treatment

Causes
-acute decrease in renal perfusion: ex. hypovolemia, decreased cardiac output, hypotension
-increased renal vascular resistance: ex. neural, humoral, pharmacologic, thromboembolic
-most common causes are decreased arterial blood pressure, increased venous pressuse or renal artery vasoconstriction
resultant decreased renal perfusion leads to compensatory mechanisms:
-inc plasma levels of norepinephrine, angiotensin II, AVP, and endothelin
-kidneys respond to increased levels of catecholamines and release prostaglandins and nitric oxide
-prostaglandins (PGE2 and prostacyclins) help maintain GFR
-nitric oxide vasodilation also helps to maintain GFR
-if COX inhibitors or ACE inhibitors used during the compensatory condition of the kidneys thet may precipitate ARF

Treatment of prerenal azotemia:
-correcting intravenous volume deficits
-improving cardiac function
-restoring normal blood pressure
-reversing the increase in renal vascular resistance

RENAL AZOTEMIA
causes
pathogenesis
oliguria vs nonoliguria
treatment

Causes
-renal ischemia about 50% of the cases (ex. hypotension, hypovolemia, impaired cardiac output)
-nephrotoxins about 35% of the cases (ex. endogenous pigments, radiographic contrast, drugs, tubular crystals)
-intrinsic renal disease about 15% of the cases (ex. glomerular disease, interstitial nephritis)

Pathogenesis
-prone to injury due to very high metabolic rate and ability to concentrate potentially toxic substances
-renal ischemia and hypoxia may likely intiate renal damage by the following pathways:
-ATP imbalance within epithelial cells due to an imbalance between oxygen supply and demand
-resultant ATP imbalance may alter ion transport which may lead to:
-altered metabolism of phospholipids and accumulation of intracellular calcium concentrations
-reperfusion injury are reoxygenation may lead to free radical mediated cellular injury
-backload of filtered solutes through damaged portions of renal tubules may allow reabsorptions of:
-creatinine, urea, and nitrogenous waste products

Oliguria vs nonoliguria ARF
nonoliguria urinary volume > 400 ml /day
oliguric urinary volume < 400 ml/ day
anuria urinary volume < 100 ml/ day

Nonoliguric ARF
-upto 50% of all cases typically have lower urinary sodium concentrations than oliguric ARF
-usually have lower complication rates and generally require shorter hospitalisation visits
-may represent less severe renal injury

Oliguric ARF
-possible to convert oliguric ARF to nonoliguric ARF with mannitol, furosemide, and 'renal doses' of dopamine (ex. 1-2 ug/kg/min)
-increases in urine output may be therapeutic by preventing tubular obstruction
-mannitol may decrease cellular swelling and free radical scaveging action

Treatment of ARF
glomerulonephritis and vasculitis may respond to supportive treatments and glucocorticosteroids
-if oliguric and anuric renal failure patients do not respond to diuretics then can try restricting fluids and electrolytes:
-fluid restriction intake to about 500 ml + urine output
-sodium restriction to about 1 mEq/kg/day intake
-potassium restriction to about 1 mEq/kg/day intake
-protein restriction to about < 0.7 g/kg/ day intake
patients with hyponatremia: treat with water restriction
patients with hypokalemia : treat with ion exchange resin ( sodium polystyrene)
glucose + insulin
calcium gluconate
possibly bicarbonate
patients with hyperphophatemia treat with dietary restrictions
phosphate binding antacids (aluminum hydroxide)
Dialysis: treat or prevent uremic complications

Indications for hemodialysis:
-fluid overload
-hyperkalemia
-drug toxicity
-severe acidosis
-pericarditis
-metabolic encephalopathy
-coagulopathy

CRRT: continous renal replacement therapy
CVVHF: continous venovenous hemofiltration
CVVHD: continous venovenous hemodialysis

POSTRENAL AZOTEMIA

general/causes
treatment

General
-caused by urinary tract obstruction
-usually obstruction to both kidneys are necessary to develop azotemia and oligura/anuria
-complete obstruction to the urinary tract eventually will lead to ARF
-prolonged partial obstruction may eventually lead to chronic renal impairment
-rapid diagnosis and relief of acute urinary obstruction usually restores normal kidney function
-physical examination normally reveals a distended urinary bladder
-abdominal x-ray may show bilateral renal calculi
-confirmation is dilation of urinary tract proximal to the site of obstruction
-commonly used studies: renal US, CT, cystoscopy with retrograde uterogram

Treatment of postrenal azotemia
-obstruction at the urinary bladder outlet: catherization of the bladder or straight suprapubic cystotomy
-ureteral obstruction : nephrostomy or utereral stent placement

Chronic Renal Failure

General
-progressive, irreversible decline in renal function
-usually occurs over a course of at least 3 - 6 months
-most common causes:
-hypertension nephrosclerosis
-diabetic nephropathy
-chronic glomerulonephritis
-polycystic renal disease

GFR
x < 25 ml/min usually manifest uremia
x < 10 ml/min usually manifest ESRD
ESRD is dependant on hemodialysis until recieving a kidney transplant

CLINICAL MANIFESTATIONS OF RENAL FAILURE

CNS:
-autonomic neuropathy
-peripheral neuropathy
-encephalopathy
-muscle twitching
-aterexis
-myoclonus
-lethargy
-confusion
-coma

CVS:
-fluid overload
-heart failure
-hypertension
-pericarditis
-arryhthmias
-conduction heart blocks
-vascular calcifications
-accelerated progression of atherosclerosis

PULMONARY:
-hyperventilation
-interstitial edema
-alveolar edema
-pleural effusion

GI:
-anorexia
-nasusea and vommiting
-hyperacidity
-mucosal ulcerations
-hemmorhage
-adynamic ileus

METABOLIC:
-metabolic acidosis
-hyperkalemia
-hyponatremia
-hypermagnesemia
-hyperphosphatemia
-hypocalcemia
-hyperuricemia
-hypoalbuminemia

HEMATOLGIC:
-anemia
-platelet dysfunction
-leukocyte dysfunction

ENDOCRINE:
-glucose intolerance
-secondary hyperparathyroidism
-hypertriglyceridemia

SKELETAL:
-ostedystrophy
-periarticular calcification

SKIN:
-hyperpigmentation
-ecchymosis
-pruritis