ARF
Uremic syndrom Uremic syndrome (uremia) is a serious complication of CRF & ARF. It occurs when urea and other waste products build up in the body because the kidneys are unable to eliminate them. These substances can become poisonous (toxic) to the body if they reach high levels.
Body system Biochemical Genatourinary GI NM Ca & skeletal Resp Hemato Cutaneous CV Manifestation Metabolic acidosis, azotemia, hprk, hprmg, Na & water retension, hprurecimia Polyurea, nocturea, protienurea Loss of libido, amenorrhea N, V, A, wt loss, amonia breath Muscle wastning, lethergy, coma hpoca, hprph, renal osteaodystrophy Dyspnea, pulmonary edema Anemai, hemolysis Pallor, pigmentation HTN, retenopathy, edema, encephalopathy
Renal calculi (kidney stones) Form mainly in the renal pelves or calyces, but can form anywhere in the kidneys Composed mainly of calcium salts, uric acid and cystine Although the exact etiology is unclear, predisposing factors include the following: Dehydration Changes in urine ph Decreased urine production Excess salt secretion Gout Obstruction of urine flow
Manifestations Many renal calculi are asymptomatic until they obstruct kidney structures such as the calyces or pelves. Severe pain that can result from obstruction Fever, chills Hematuria Gastrointestinal symptoms (nausea, vomiting) Urine obstruction Complications that may include damage to renal structures and acute renal failure
Renal tumors Tumors of the kidney may be either rare benign adenomas or, more commonly, malignant renal cell carcinomas. If benign adenomas arise, they tend to be small and usually not clinically significant. The prognosis for renal cell carcinomas depends upon the morphology of the cells involved and the extent of spread outside the kidney. Renal carcinomas may metastasize to the lymphatics, liver, lungs and bone marrow.
Manifestations Hematuria Flank pain Weight loss Many renal tumours asymptomatic until the tumour is of advanced size and begins to disrupt renal structures Metastatic tumours that can occur with advanced disease
Wilm s tumour (nephroblastoma) Rare malignant tumour that arises in infants and children. The tumour presents with unique histology that may resemble embryonic kidney. Tumour can metastasize rapidly.
Introduction Abrupt decrease in renal function. The causes of acute renal failure may be prerenal, intrarenal or postrenal in nature. Acute renal failure is often reversible so long as permanent injury to the kidney has not occurred.
Introduction Decreased GFR causes Cr to rise as much as 0.5 mg/dl/d & BUN as much as 10 mg/dl/d over a period of several days.
General notes The renal protective effect of PG can be negated by the administration of NSAIDs. ACEI may also precipitate ARF under conditions of renal hypoperfusion. ATN arise from either prolonged renal ischemia or exposure to nephrotoxine. The terms ATN & ARF are used interchangably which is incorrect.
General notes ATN refers to a type of lesion that is common but not always associated with ARF. ARF may be present without ATN as in malignant HTN allergic rxs ect. Nephrotoxic sub include: methanol, ethylene glycole, inhalation of CCL4. Endogenous nephrotoxines include Hgb, myoglobin
Manifestations S & S similar to those of uremic syndrome in CRF, reflecting failure of the kidneys regulatory, excretory, and endocrine functions. However anemia and osteodystrophy are not common because of its acute onset.
Manifestations Oliguria (reduced urine output) Possible edema and fluid retention Elevated blood urea nitrogen levels (BUN) and serum creatinine Alterations in serum electrolytes
Clinical course of ARF Oliguric stage: the clinical feature is often dominated by surgical, medical, or obstetric calamity causing renal injury. This stage is usually present with in 24-28 hrs after the initial injury. Azotemia accompany this stage (S&S appear after several days) The average duration of this stage is from 7-10 d, there is rise in BUN & Cr. In general patient with non-oliguric ARF have better prognosis than those with oliguric ARF.
Clinical course of ARF diuretic stage: the stage begins when urine output increase to more than 400 ml/d. The high urine volume is due to osmotic diureses produced by high urea conc and impaired ability to conserve filtered salts and water. Patient may develop deficits of potassium, sodium and water. In the beginning BUN may rise the azotemia gradually disappears and there is great clinical improvement.
Clinical course of ARF recovery stage: the recovery lasts as long as one year, some patients are however left with permanent reduction of GFR.
Pathophysiology of ARF Several theory's have been proposed: 1. Tubular obstruction. 2. Backleak of tubular fluid. 3. Decreased golmarular permeability. 4. Vasomotor dysfunction. 5. Tubuloglomerular feedback.
Tubular obstruction ATN lead to desquamation of nephrotic tubular cells & other material which then form casts and occlude the tubule, also cellular swelling as a result of ischemia, net GFR is reduced, like in ARF caused by heavy metals
Backleak of tubular fluid GF continues normally but tubular fluid leaks out of the lumina through damaged tubular cells to the peritubular circulation.
Decreased golmarular permeability Glomarular capillary endothelial cells undergoes changes that reduce permeability or surface area of filtration.
Vasomotor dysfunction Intrarenal distribution of blood flow from the cortex to the medulla during acute & prolonged hypotension. So there is relative ischemia of renal cortex. Constrection of affrent arteriols provide a vascular bases for the marked reduction GFR. Renal ischemia would then activate the reninangiotensin system and perpetuate cortical ischemia after the initial stimulus has disappeared. Some authors have postulated PG role in VMD in ARF since PG inhibitors as aspirin reduce renal blood flow and potentiate ATN.
Tubuloglomerular feedback A phenomena in which the flow to the distal nephrones is regulated by receptors in the macula densa of the distal tubules which lies in proximity to the glomarular pole. If distal flow is incr the reabsorpative capacity of distal tubules and collecting ducts could be over whelmed and lead to ECF depletion. Thus decreased GFR by TGF could be considered as an adaptive mechanism.