-Acute Renal Failure-
-Acute renal failure has largely been replaced by the term acute kidney injury
-Acute renal failure is characterized the abrupt loss of kidney function resulting in the retention of urea and other nitrogenous waste products and in the dysregulation of extracellular volume and electrolytes
-The loss of kidney function is most easily detected by an elevation of serum creatinine which is used to estimate glomerular filtration rate
-Have to decide etiology of renal failure pre-renal, intrinsic, or post renal obstruction
-Pre-Renal causes of renal failure include: hemorrhage, volume depletion, fluid pooling, relative decrease in blood volume (ineffective arterial volume) and arterial occlusion
-Intrinsic causes include: vascular (vasculitis), acute glomerular nephritis, acute interstitial nephritis, acute tubular necrosis
-Post Obstructive causes include bladder outlet obstruction, bilateral ureter obstruction, ureteral obstruction in a solitary kidney
-workup should include urinalysis, urine indices, bladder catheterization, renal ultrasound, and perhaps renal biopsy
-If etiology is post renal or pre renal, therapy should be targeted at reversing the etiology. Volume replacement, anticoagulation for arterial occlusion, or blood replacement for pre renal causes. Removing or diverting the post renal obstruction is the target of treatment for post renal obstruction.
-Treating the intrinsic cause if possible is the key for targeting intrinsic renal failure
-Acute renal failure is characterized the abrupt loss of kidney function resulting in the retention of urea and other nitrogenous waste products and in the dysregulation of extracellular volume and electrolytes
-The loss of kidney function is most easily detected by an elevation of serum creatinine which is used to estimate glomerular filtration rate
-Have to decide etiology of renal failure pre-renal, intrinsic, or post renal obstruction
-Pre-Renal causes of renal failure include: hemorrhage, volume depletion, fluid pooling, relative decrease in blood volume (ineffective arterial volume) and arterial occlusion
-Intrinsic causes include: vascular (vasculitis), acute glomerular nephritis, acute interstitial nephritis, acute tubular necrosis
-Post Obstructive causes include bladder outlet obstruction, bilateral ureter obstruction, ureteral obstruction in a solitary kidney
-workup should include urinalysis, urine indices, bladder catheterization, renal ultrasound, and perhaps renal biopsy
-If etiology is post renal or pre renal, therapy should be targeted at reversing the etiology. Volume replacement, anticoagulation for arterial occlusion, or blood replacement for pre renal causes. Removing or diverting the post renal obstruction is the target of treatment for post renal obstruction.
-Treating the intrinsic cause if possible is the key for targeting intrinsic renal failure
-The RIFLE criteria consists of 3 graded levels of kidney dysfunction (risk, injury, and failure)
-Risk(Stage 1)-1.5 increase in serum creatinine or GFR decrease by 25 percent or urine output less than 0.5 mL/kg per hour for 6 hours
-Injury (Stage 2)-Two fold increase in serum creatinine or GFR decrease by 50 percent or urine output less than 0.5 mL/kg for 12 hours
-Failure (Stage 3)-threefold increase in serum creatinine or GFR decrease by 75 percent or urine output of less than 0.3 mL/kg for 12 hours or anuria
-End Stage Renal Disease- complete loss of kidney function for more than 3 months
-Chronic Kidney Disease-
-Risk(Stage 1)-1.5 increase in serum creatinine or GFR decrease by 25 percent or urine output less than 0.5 mL/kg per hour for 6 hours
-Injury (Stage 2)-Two fold increase in serum creatinine or GFR decrease by 50 percent or urine output less than 0.5 mL/kg for 12 hours
-Failure (Stage 3)-threefold increase in serum creatinine or GFR decrease by 75 percent or urine output of less than 0.3 mL/kg for 12 hours or anuria
-End Stage Renal Disease- complete loss of kidney function for more than 3 months
-Chronic Kidney Disease-
-Chronic kidney disease is a group of heterogenous disorders characterized by alterations of kidney structure and function which manifest in ways depending on the underlying cause and the severity of disease
-Chronic kidney disease is defined by the presence of kidney damage or decreased kidney function for 3 or more months
-End stage renal disease refers to kidney failure treated with either dialysis or transplantation
-Kidney damage is identified most cases by one of the following kidney markers: albuminuria, urine sediment abnormalities, imaging abnormalities (PCKD), pathologic abnormalities (glomerular or vascular disease)
-GFR is considered to be the best index of overall kidney function. Decreasing GFR is characteristic of progressive kidney disease
-G1 is a GFR greater than 90% normal to high
-G2 is a GFR 60-89% mildly decreased
-G3a is a GFR 45-59% mild to moderately decreased
-G3b is a GFR 30-44% moderately to severely decreased
-G4 is a GFR 15-29% severely decreased
-G5 is a GFR less than 15% kidney failure
-Treatment of chronic kidney disease includes treatment of reversible causes of renal failure, preventing or decreasing progression of disease, treating the complications of renal failure, adjusting drug doses for GFR.
-Reversible causes of renal failure include improving decreased renal perfusion, stopping nephrotoxic medications, and relieving urinary tract obstruction
-Renal perfusion can be decreased by hypovolemia (vomiting, bleeding diuretic use), infections such as sepsis, NSAIDS and ACE inhibitors
-Nephrotoxic meds include aminoglycoside antibiotics, NSAIDS, IV contrast dye
-If urinary tract obstruction, need to target therapy to remove it
-Ways to help decrease using ACE inhibitors or Angiotensin Receptor Blockers, protein restriction, statin therapy, smoking sensation, and treatment of chronic metabolic acidosis with supplemental bicarbonate
-Complications of renal failure include volume overload, hyperkalemia, metabolic acidosis, anemia, hypertension, mineral and bone disorders
-Anemia can happen from decreased erythropoetin
-Hyperphosphatemia happens becomes of decreased reduction in the filtered phosphate load
-Glomerulonephritis-
-Two major changes in the urine distinguish glomerulonephritis: hematuria with RBC casts and proteinuria exceeding 3.5 grams per day
-Glomerulonephritis classification can be described according to causes, pathologic lesions, disease presentation, or clinical presentation
-Post-Streptococcal Glomerulonephritis causes diffuse lesions usually occurs 7-10 days after a streptococcal infection (Group A Beta Hemolytic Streptococcus). Serum complement levels are low. Presents with hematuria, RBC casts, proteinuria, oliguria, edema, and hypertension. Most people recover without significant loss of renal function
-Rapidly Progressing Glomerulonephritis-also know as subacute, crescentic, or extra papillary glomerulonephritis. Usually affects people in their 50's and 60's. Can be idiopathic or associated with proliferative glomerular diseases such as post streptococcal glomerular nephritis and Good Pasteur Syndrome. ANCA antibodies associated with vasculitis are common with this disease. Dialysis or Renal Transplant is often needed when not reversible
-Membranoproliferative Glomerulonephritis-usually idiopathic and associated with hypocomplementemia. Affect basement membrane and causes diffuse lesions
-IgA Nephropathy (Berger's Disease) usually idiopathic and get elevated IgA levels. Usually focal involvement
-Minimal Change Disease (Lipoid Nephrosis) usually idiopathic and causes diffuse fusion of epithelial foot processes due to loss of negative charge in basement membrane and increase permeability lead to severe proteinuria and nephritic syndrome
-Focal Glomerulosclerosis- usually idiopathic and similar to minimal change disease. Difference is there is hyaline deposits that lead to increased permeability of the glomerular membrane.
-Membranous Nephropathy- usually idiopathic but can be associated with systemic diseases such as hepatitis B, SLE, and solid malignant tumors. Causes diffuse thickening of the glomerular basement membrane and capillary walls from deposits of antibody and complement.
-Hydronephrosis-
-hydronephrosis is usually due to a urinary tract obstruction
-hydronephrosis can be due to pregnancy or a large diuresis. Can also see with nephrogenic diabetes insipidus
-hydronephrosis can be unilateral or bilateral
-Bilateral hydronephrosis is usually due to urinary tract outflow obstruction such as prostatitis, urinary retention, strictures caused by radiation to the pelvis, or pelvic mass
-Unilateral hydronephrosis is usually due to kidney stone but also can be from tumor.
-Treatment of hydronephrosis is to remove the obstruction
-Nephrotic Syndrome-
-Nephrotic syndrome means the presence of heavy proteinuria (greater than 3.5 grams in 24 hours) hypoalbuminemia (less than 3.0 grams/dL) and peripheral edema. Hyperlipidemia and thrombotic disease is often associated with it.
-Patients with heavy proteinuria without edema or hypoalbuminemia is suggestive of focal segmental glomerulosclerosis
-Minimal change disease is the most predominant cause of nephrotic syndrome in children
-In adults 30 percent will have systemic disease such as diabetes mellitus, amyloidosis, or SLE
-Focal segmental glomerulosclerosis is the most common lesion found to be seen in adults with nephrotic syndrome
-Membranous Nephropathy is the most common cause of primary nephrotic syndrome in adults. It is characterized by basement membrane thickening due to autoantibodies
-Amyloidosis-is suspected when there is a history of chronic inflammatory disease or detection of the monoclonal paraprotein in the serum or urine
-Polycystic Kidney Disease-
-Autosomal dominant polycystic kidney disease occurs in 1 in every 400-1000 live births.
-Less than one half of the persons effected will be diagnosed because the diseases is often clinically silent
-Diagnosis is made on imaging of kidney, usually by ultrasound or by CT scan of Abdomen and Pelvis
-Typically find large kidneys with extensive cysts throughout both kidneys
-Genetic testing is required for definite diagnosis
-Family history is important for screening for this disorder. Ultrasound is the safest modality for screening for this disorder
-Affected patients may present with flank pain, renal insufficiency and hypertension. Patients may also have cysts in their pancreas or liver
-autosomal recessive polycystic kidney disease (infantile polycystic kidney disease) causes cystic dilations of the renal collecting ducts and congenital hepatic fibrosis
-pulmonary insufficiency is a major cause of death for patients with ARPKD. The infants typically have pulmonary hypoplasia.
-diagnosis of ARPKD is based on clinically findings, imaging and lab findings. Genetic testing can aid in the diagnosis
-Management of ARPKD is supportive. Patients will need dialysis and or transplantation
-Renal Vascular Disease-
-Renal vascular disease is a correctable cause of secondary hypertension
-Renal vascular disease accounts for 1 percent of the cases of mild to moderate elevations of blood pressure
-Indications for testing include findings suggest a cause of secondary hypertension, the patients does not appear to have a cause of secondary hypertension such as primary kidney disease, primary aldosteronism, or pheochromocytoma, or an intervention is planned for a stenotic lesion
-The gold standard for diagnosis renal vascular disease is renal angiography
-Less invasive testing includes duplex doppler ultrasonography, CTA of Renal Arteries, MRA of Renal Arteries
-Plasma renin activity is only elevated in only 50-80 percent of patients with renal hypertension
-Ultimately treatment of renal vascular disease is done with intervention through renal angiography
-Chronic kidney disease is defined by the presence of kidney damage or decreased kidney function for 3 or more months
-End stage renal disease refers to kidney failure treated with either dialysis or transplantation
-Kidney damage is identified most cases by one of the following kidney markers: albuminuria, urine sediment abnormalities, imaging abnormalities (PCKD), pathologic abnormalities (glomerular or vascular disease)
-GFR is considered to be the best index of overall kidney function. Decreasing GFR is characteristic of progressive kidney disease
-G1 is a GFR greater than 90% normal to high
-G2 is a GFR 60-89% mildly decreased
-G3a is a GFR 45-59% mild to moderately decreased
-G3b is a GFR 30-44% moderately to severely decreased
-G4 is a GFR 15-29% severely decreased
-G5 is a GFR less than 15% kidney failure
-Treatment of chronic kidney disease includes treatment of reversible causes of renal failure, preventing or decreasing progression of disease, treating the complications of renal failure, adjusting drug doses for GFR.
-Reversible causes of renal failure include improving decreased renal perfusion, stopping nephrotoxic medications, and relieving urinary tract obstruction
-Renal perfusion can be decreased by hypovolemia (vomiting, bleeding diuretic use), infections such as sepsis, NSAIDS and ACE inhibitors
-Nephrotoxic meds include aminoglycoside antibiotics, NSAIDS, IV contrast dye
-If urinary tract obstruction, need to target therapy to remove it
-Ways to help decrease using ACE inhibitors or Angiotensin Receptor Blockers, protein restriction, statin therapy, smoking sensation, and treatment of chronic metabolic acidosis with supplemental bicarbonate
-Complications of renal failure include volume overload, hyperkalemia, metabolic acidosis, anemia, hypertension, mineral and bone disorders
-Anemia can happen from decreased erythropoetin
-Hyperphosphatemia happens becomes of decreased reduction in the filtered phosphate load
-Glomerulonephritis-
-Two major changes in the urine distinguish glomerulonephritis: hematuria with RBC casts and proteinuria exceeding 3.5 grams per day
-Glomerulonephritis classification can be described according to causes, pathologic lesions, disease presentation, or clinical presentation
-Post-Streptococcal Glomerulonephritis causes diffuse lesions usually occurs 7-10 days after a streptococcal infection (Group A Beta Hemolytic Streptococcus). Serum complement levels are low. Presents with hematuria, RBC casts, proteinuria, oliguria, edema, and hypertension. Most people recover without significant loss of renal function
-Rapidly Progressing Glomerulonephritis-also know as subacute, crescentic, or extra papillary glomerulonephritis. Usually affects people in their 50's and 60's. Can be idiopathic or associated with proliferative glomerular diseases such as post streptococcal glomerular nephritis and Good Pasteur Syndrome. ANCA antibodies associated with vasculitis are common with this disease. Dialysis or Renal Transplant is often needed when not reversible
-Membranoproliferative Glomerulonephritis-usually idiopathic and associated with hypocomplementemia. Affect basement membrane and causes diffuse lesions
-IgA Nephropathy (Berger's Disease) usually idiopathic and get elevated IgA levels. Usually focal involvement
-Minimal Change Disease (Lipoid Nephrosis) usually idiopathic and causes diffuse fusion of epithelial foot processes due to loss of negative charge in basement membrane and increase permeability lead to severe proteinuria and nephritic syndrome
-Focal Glomerulosclerosis- usually idiopathic and similar to minimal change disease. Difference is there is hyaline deposits that lead to increased permeability of the glomerular membrane.
-Membranous Nephropathy- usually idiopathic but can be associated with systemic diseases such as hepatitis B, SLE, and solid malignant tumors. Causes diffuse thickening of the glomerular basement membrane and capillary walls from deposits of antibody and complement.
-Hydronephrosis-
-hydronephrosis is usually due to a urinary tract obstruction
-hydronephrosis can be due to pregnancy or a large diuresis. Can also see with nephrogenic diabetes insipidus
-hydronephrosis can be unilateral or bilateral
-Bilateral hydronephrosis is usually due to urinary tract outflow obstruction such as prostatitis, urinary retention, strictures caused by radiation to the pelvis, or pelvic mass
-Unilateral hydronephrosis is usually due to kidney stone but also can be from tumor.
-Treatment of hydronephrosis is to remove the obstruction
-Nephrotic Syndrome-
-Nephrotic syndrome means the presence of heavy proteinuria (greater than 3.5 grams in 24 hours) hypoalbuminemia (less than 3.0 grams/dL) and peripheral edema. Hyperlipidemia and thrombotic disease is often associated with it.
-Patients with heavy proteinuria without edema or hypoalbuminemia is suggestive of focal segmental glomerulosclerosis
-Minimal change disease is the most predominant cause of nephrotic syndrome in children
-In adults 30 percent will have systemic disease such as diabetes mellitus, amyloidosis, or SLE
-Focal segmental glomerulosclerosis is the most common lesion found to be seen in adults with nephrotic syndrome
-Membranous Nephropathy is the most common cause of primary nephrotic syndrome in adults. It is characterized by basement membrane thickening due to autoantibodies
-Amyloidosis-is suspected when there is a history of chronic inflammatory disease or detection of the monoclonal paraprotein in the serum or urine
-Polycystic Kidney Disease-
-Autosomal dominant polycystic kidney disease occurs in 1 in every 400-1000 live births.
-Less than one half of the persons effected will be diagnosed because the diseases is often clinically silent
-Diagnosis is made on imaging of kidney, usually by ultrasound or by CT scan of Abdomen and Pelvis
-Typically find large kidneys with extensive cysts throughout both kidneys
-Genetic testing is required for definite diagnosis
-Family history is important for screening for this disorder. Ultrasound is the safest modality for screening for this disorder
-Affected patients may present with flank pain, renal insufficiency and hypertension. Patients may also have cysts in their pancreas or liver
-autosomal recessive polycystic kidney disease (infantile polycystic kidney disease) causes cystic dilations of the renal collecting ducts and congenital hepatic fibrosis
-pulmonary insufficiency is a major cause of death for patients with ARPKD. The infants typically have pulmonary hypoplasia.
-diagnosis of ARPKD is based on clinically findings, imaging and lab findings. Genetic testing can aid in the diagnosis
-Management of ARPKD is supportive. Patients will need dialysis and or transplantation
-Renal Vascular Disease-
-Renal vascular disease is a correctable cause of secondary hypertension
-Renal vascular disease accounts for 1 percent of the cases of mild to moderate elevations of blood pressure
-Indications for testing include findings suggest a cause of secondary hypertension, the patients does not appear to have a cause of secondary hypertension such as primary kidney disease, primary aldosteronism, or pheochromocytoma, or an intervention is planned for a stenotic lesion
-The gold standard for diagnosis renal vascular disease is renal angiography
-Less invasive testing includes duplex doppler ultrasonography, CTA of Renal Arteries, MRA of Renal Arteries
-Plasma renin activity is only elevated in only 50-80 percent of patients with renal hypertension
-Ultimately treatment of renal vascular disease is done with intervention through renal angiography
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