Renal Diseases-CMA.A
Poststreptococcal glomerulonephritis (PSGN) is Bacterial glomerulonephritis
is caused by prior infection with specific nephritogenic strains of group A beta-hemolytic streptococcus.
Glomerulonephritis glomeruli-cluster of capillaries around the end of a kidney tubule, where waste products are filtered from the blood.
is inflammation of the tiny filters in your kidneys (glomeruli). Glomeruli remove excess fluid, electrolytes and waste from your bloodstream and pass them into your urine. Also called glomerular disease, glomerulonephritis can be acute — a sudden attack of inflammation — or chronic — coming on gradually.
cystine stones
occur with inherited transport disorder cystinuria
Nephrotic syndrome (NS) etiology most common cause is membranous GN-the majority of children with NS have minimal change disease
primary glomerular disease (all subtypes) infection (PSGN) Drugs (NSAIDS, penicillamine, and gold) neolasia (Hodgkin's lyphoma); Multisystm diseas (SLE, Good pature's syndrome, Endocrine disease (DM), Miscellaneous (preeclampic toxemia)
kidney stones classical finding Diagnostic TEST: use helical CT for identifying the retained stones
rental colic sudden, sever, flank pain with radiating to the groin,----Hematuria--- frequency, urgency, dysuria and relief following stone passage
Non Poststreptococcal glomerulonephritis (NPSGN) TREATMENT
***symptomatic treatment with protein restriction, fluid restriction, low salt intake and loop diuretic plus CORTICOSTERIODS
Poststreptococcal glomerulonephritis (PSGN) TREATMENT diuretic-three types of diuretics: thiazide, loop and potassium-sparing. Each works by affecting a different part of your kidneys, and each may have different uses, side effects and precautions.
***symptomatic treatment with protein restriction, fluid restriction, low salt intake and loop diuretic- ****penicillin eradicates the group A BETA hemolytic Streptococcus but will not affect the course of the GN
Glomerulonephritis signs and symptoms may include: clinical finding: maybe asymptomatic more severe cases: malaise, headache, anorexia, mild fever, flank pain, proteinuria, edema, impaired renal function, hypertention, pulmonary edema may occur, oliguria with bloody, coffee colored or smoke
*Pink or cola-colored urine from red blood cells in your urine (hematuria) *Foamy urine due to excess protein (proteinuria) *High blood pressure (hypertension) *Fluid retention (edema) with swelling evident in face, hands, feet and abdomen *Fatigue from anemia or kidney failure (according to mayo clinic) NOTE: SOME STRAINS DO NOT PRODUCE STREPTOLYSIN- a streptococcal hemolytic exotoxin
Glomerulonephritis classification incidence: > 50% of cases are children < 13 yo predominantly age of 2 and 10 years cause: Streptococcal infection as the most common cause of Acute glomerulonephritis
1. Acute -PSGN 2. NPSGN- many subgroups
Nephrotic syndrome CLINICAL FINDING
Edema, proteinurial (> 35 g/day) hypoalbuminemia, hypertension, hyperlipidemia, and renal insufficiency
What causes anemia in chronic kidney disease? Other common causes of anemia in people with kidney disease include blood loss from hemodialysis and low levels of the following nutrients found in food: iron, vitamin B12, folic acid
When kidneys are diseased or damaged, they do not make enough EPO. As a result, the bone marrow makes fewer red blood cells, causing anemia. When blood has fewer red blood cells, it deprives the body of the oxygen it needs. These nutrients are necessary for red blood cells to make hemoglobin, the main oxygen-carrying protein in the red blood cells.
Nephrotic syndrome -PHARMACOLOGIC TREATMENT
a. loop diuretic b. ACE inhibitors c. anticoagulant d. prednison e. cytotoxic agents
Glomerulonephritis pathogenesis Pathognomonic clue in Acute GN is red blood cell casts, other notable abnormalities are increased ESR and ASO titer
the syndrome may begin as early as 1 week after the initial streptococcal infection. usually patient presents with diffuse proliferation G.N. NOTE: SOME STRAINS DO NOT PRODUCE STREPTOLYSIN- a streptococcal hemolytic exotoxin
Infectious stones
urea splitting organism (proteus species) prevention: the stone should be removed completely and antibiotic treatment -drink enough liquid daily
calcium oxalate stones (most frequent) cause
usually idiopathic and associated with hypercalciuria, hyperuricura and hypocitraturia
uric acid stones (second most common) cause Prevention : make urine alkaline by taking bicarbonate or citrate and use allopurinal-decrease purin intake, red meat, animal organs, eg liver, kidney or sweetbread/beans
associated with persistence acidic urine and in conjunction with massively incread urinary uric acid secretion ( >1000 mg/day)
Renal stones types of stones: prevention: restrict intake of animal protein and salt combined with normal protein and salt combined with normal calcium intake is recommended for preventing recurrent hypercalciuria
calcium oxalate stones (most frequent) and uric acid stones (second most common)
acute pyelonephritis
complications or comilicating disease should be hospitalized, no complication, treat the patients as outpatient, use IV port therapy dialy or high dose oral threapy Prophylaxis for high risk patients with first choice quinolones or Marcodantin
Chronic renal failure (CRF) clinical finding
weakness, fatigue, headache, anorexia, nausea, pruritus, polyuria, nocturia, edema, HTN, CHF, Pericarditis, anemia, azotemia, acidosis, hyperkalemia, hpocalcermia, hyperphosphatemia
How is anemia related to CHRONIC RENAL FAILURE: Anemia commonly occurs in people with chronic kidney disease (CKD)—
—the permanent, partial loss of kidney function. Anemia might begin to develop in the early stages of CKD, when someone has 20 to 50 percent of normal kidney function.
Chronic renal failure cause: most common cause is Diabetes mellitus with prevalence of DM type II is 10x more than DM type1. *****The logical conclusion is that DM type II is common cause of chronic RF than DM type I
describes the gradual loss of kidney function. Your kidneys filter wastes and excess fluids from your blood, which are then excreted in your urine. When chronic kidney disease reaches an advanced stage, dangerous levels of fluid, electrolytes and wastes can build up in your body.
the clinical presentation of PSGN varies
from asymptomatic, microscopic hematuria to the full-blown acute nephritic syndrome, characterized by red to brown urine, proteinuria (which can reach the nephrotic range), edema, hypertension, and acute kidney injury. The prognosis is generally favorable, especially in children, but in some cases, the long-term prognosis is not benign.
Nephrotic syndrome NON-PHARMACOLOGIC TREATMENT
Sodium restriction and fluid restriction
Glomerulonephritis cause
Streptococcal infection as the most common cause of Acute Glomerulonephritis
Anemia tends to worsen as CKD progresses. Most people who have total loss of kidney function, or kidney failure, have anemia.1 A person has kidney failure when he or she needs a kidney transplant or dialysis in order to live.
The two forms of dialysis include hemodialysis and peritoneal dialysis. Hemodialysis uses a machine to circulate a person's blood through a filter outside the body. Peritoneal dialysis uses the lining of the abdomen to filter blood inside the body.
Complications includes
Hypertensive encephalolopathy-CHF Acute RENTAL FAILURE and CHRONIC RENAL INFECTION -neuropathic syndromes
glomerulonephritis prognosis
90% of PSGN patients recover renal function within 8 to 12 weeks Excellent prognosis in patient with minimal change. > 70% of patient with mesangial capillary GN will develop chronic renal failure
Chronic renal failure (CRF) pharmacological treatment Adjust certain drug does to correct for prolonged half life
ACE inhibitors Adrenergic receptor binders (ARBs) Nondihydropyrides calculm calcium channel blockers/control HTN Erythropoietin -loop diuretic Correct electrolytes abnormalities HMG CoA reductase inhibitors other: hemodialysis. peritoneal dialysis, renal transplantation
STONE TREATMENT
Calcium oxalate stones-maintain normal calcium intake with meals-restrict dietary sodium to 2 g/day (6 g of salt/day)-limit intake protein and carbohydrates -use oral orthophosphates to decrease stone forming potential -use thiazide diuretics-use allopurinol and urinary alkalinization to reduce the formation of urate crystal
Chronic renal failure (CRF) treatment
NON pharmacologic treatment: restrict protein, maintain careful fluid balance, restrict sodium, potassisum and phosphate, avoid potential renal toxic drug (NSAID), calcium and vitamin D supplement
Chronic renal failure (CRF) lab test
Serum Creatine reaches 200-300 micro mol/L or 2-3 mg/L, GFR decreased to 20-30 ml/min
