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Atin

Category: Blood Pressure

Description

Tenormin is used to treat angina (chest pain) and hypertension (high blood pressure). It is also used to treat or prevent heart attack.

Active Ingredient: Atenolol

Tenormin (Atin) as known as: Alcenol, Almylar, Aminol, Amlowide, Angipress, Anlipin, Anol, Anselol, Antipressan, Apo-atenolol, Atebeta, Atebloc, Ateblocor, Atecard, Atecor, Atehexal, Ateloc, Aten, Atendal, Atenemeal, Atenet, Atenex, Ateni, Atenil, Atenix, Ateno, Ateno-isis, Atenobal, Atenobene, Atenoblock, Atenocor, Atenodan, Atenodeks, Atenogamma, Atenogen, Atenol, Atenolan, Atenololum, Atenomel, Atenopress, Atenor, Atenorhythm, Atenosafe, Atenovit, Atermin, Atestad, Athenol, Atin, Atoken, Atol, Atormin, Atpure, Azectol, Beta-adalat, Beta-bloquin, Betablock, Betabloquin, Betacard, Betanex, Betanol, Betasec, Betaten, Betatop, Bio-atenolol, Biofilen, Blikonol, Blocotenol, Blokanol, Blokium, Blotex, Bpnol, Canar, Cardaten, Cardaxen, Cardilock, Cardiotal, Cardipro, Catenol, Clortanol, Coratol, Corin, Corotenol, Docateno, Docatone, Dolru, Durabeta, Enol, Ephitensin, Etnol, Fabotenol, Farnormin, Fealin, Fellfish, Felobits, Hipress, Ibinolo, Internolol, Jenatenol, Juvental, Katenomin, Kushisemin, Labotensil, Lismories, Lonet, Lonol, Lopres, Lorten, Loten, Mecrol, Mesonex, Metinin, Mezarid, Mezolmin, Mirobect, Myocord, Neatenol, Normalol, Normaten, Normitab, Normiten, Normocard, Nortan, Nortenolol, Noten, Novo-atenol, Originol, Ormidol, Panapres, Plenacor, Pms-atenolol, Precinol, Prenolol, Prenormine, Prinorm, Savetens, Schein, Selobloc, Synarome, Tanser, Telvodin, Temoret, Tenblok, Tenoblock, Tenocar, Tenocor, Tenol, Tenoloc, Tenolol, Tenomax, Tenomilol, Tenoprin, Tenoren, Tenoret, Tenoretic, Ténormine, Tenostat, Tensig, Tensimin, Tensinor, Tensol, Tensotin, Tessifol, Therabloc, Totamol, Towamin, Tozolden, Trantalol, Tredol, Umoder, Uniloc, Vascoten, Velorin, Vericordin, Zumablok

Approved» - Сторінка 13

In drug-induced ATIN, renal function usually recovers within 6 to 8 wk when the offending drug is withdrawn, although some residual scarring is common. Recovery may be incomplete, with persistent azotemia above baseline. When other factors cause ATIN, histologic changes usually are reversible if the cause is recognized and removed; however, some severe cases progress to fibrosis and renal failure. Regardless of cause, diffuse rather than patchy interstitial infiltrates, delayed response to prednisone, and persistent acute renal failure (> 3 wk) suggest irreversible injury. In CTIN, prognosis depends on the cause and on the ability to recognize and stop the process before irreversible fibrosis occurs. Many genetic (cystic kidney disease), metabolic (cystinosis), and toxic (heavy metal) causes may not be modifiable, in which case CTIN usually evolves to end-stage renal disease.

Treatment of both ATIN and CTIN is management of the underlying causes. For immunologically induced disease in ATIN and perhaps CTIN, corticosteroids (eg, prednisone 1 mg/kg po once/day for 3 days and decreased over the next 7 to 10 days) may accelerate recovery. Also in patients with CTIN and progressive renal insufficiency, ACE inhibitors or angiotensin receptor blockers may slow disease progression.


Analgesic Abuse Nephropathy


Analgesic abuse nephropathy (AAN) is CTIN caused by cumulative lifetime use of large amounts (eg, > 2 kg) of certain analgesics.

AAN was originally described in conjunction with overuse of combination analgesics containing phenacetin (typically with aspirin, acetaminophen, codeine, or caffeine). However, despite removal of phenacetin from the market, AAN continued to occur. Studies to identify the causal agent are equivocal, but acetaminophen, aspirin, and other NSAIDs have been implicated. Mechanism is unclear. Whether COX-2 inhibitors cause AAN is not known, but these drugs probably can cause ATIN and nephrotic syndrome due to minimal change disease or membranous nephropathy.

AAN predominates in women (peak incidence, 50 to 55 yr) and, in the US, is responsible for 3 to 5% of cases of end-stage renal disease (13 to 20% in Australia and South Africa).

Patients present with renal insufficiency, a bland urinary sediment, and non-nephrotic proteinuria. Hypertension and impaired urinary concentration are common. Flank pain and hematuria are signs of papillary necrosis that occur late in the course of disease. Chronic complaints of musculoskeletal pain, headache, malaise, and dyspepsia may be precipitants of long-term analgesic use rather than effects of AAN.

Diagnosis is based on history and noncon-trast CT. CT signs of A AN are decreased renal size; "bumpy" contours, defined as at least 3 indentations in the normally convex outline of the kidney; and papillary calcifications, which have a sensitivity of 92% and a specificity of 100% for early diagnosis.

Renal function stabilizes when analgesics are stopped unless renal insufficiency is advanced, in which case it may progress to renal failure. Patients with AAN are at greater risk of transitional cell carcinomas of the urinary tract.

Acute urate nephropathy: This is not a true form of ATIN but rather an intraluminal obstructive uropathy caused by uric acid crystal deposition within the lumen of renal tubules; acute oliguric or anuric renal failure results. It most commonly occurs from tumor lysis syndrome after treatment of lymphoma, leukemia, or other myeloproliferative diseases, but it also occurs after seizures or treatment of solid tumors and with rare primary disorders of urate overproduction (hypoxanthine-guanine phosphoribo-syltransferase deficiency) or overexcretion due to decreased proximal tubule reabsorption (Fanconi-like syndromes).

Diagnosis is suspected when acute renal failure (ARF) occurs with marked hyperuricemia (> 15 mg/dL). Typically, no symptoms are present. Urinalysis may be normal or may show urate crystals.

Prognosis for complete recovery of renal function is excellent if treatment is initiated rapidly. Treatment is supportive and may include hemodialysis to remove excess circulating urate in severe cases where diuresis cannot be induced with a loop diuretic and IV saline.

Prevention is by alkalinization of the urine to pH > 6.5 and use of allopurinol 300 mg bid to tid plus saline loading to maintain a urine output > 2.5 L/day before chemotherapy or radiation therapy. Urate oxidase (rasburicase), which catalyzes urate to a much more soluble compound, is also preventative but is not widely used because it must be given IV and can cause anaphylaxis, hemolysis, and other adverse effects.

Chronic urate nephropathy: This condition is CTIN caused by deposition of Na urate crystals in the medullary interstitium in the setting of chronic hyperuricemia. Sequelae are chronic inflammation and fibrosis, with ensuing chronic renal insufficiency and renal failure. Chronic urate nephropathy was once common in patients with tophaceous gout but is now rare because of treatment. A bland urine sediment and hyperuricemia disproportionate to the degree of renal insufficiency (eg, urate > 9 mg/dL with serum creatinine 10 mg/dL with serum creatinine 1.5 to 2 mg/dL, and > 12 mg/dL with more advanced renal failure) are suggestive but nonspecific; many causes of tubulointerstitial diseases may have these findings, lead nephropathy being the most common (see below). Treatment is that of hyperuricosuria.

Hyperoxaluria: Hyperoxaluria is a cause of both acute and chronic tubulointerstitial nephritis. ATIN and ARF may develop in susceptible patients who ingest high-oxalate foods (eg, tea, chocolate, spinach, rhubarb, star fruit) or who are exposed to exogenous substances that are metabolized into oxalate (eg, ethylene glycol ingestion, methoxyflurane anesthesia, large doses of ascorbic acid). CTIN and progressive chronic renal failure develop in patients with inherited disorders of excessive oxalate production (types I and II primary hyperoxaluria) or acquired GI diseases (eg, short bowel syndrome with increased gut absorption). Oxalate is highly insoluble when combined with Ca, and urinary excretion of greater than normal amounts leads to Ca oxalate precipitation and subsequent nephrolithiasis, ARF, or tubulointerstitial damage. Symptoms and signs differ by form of disease and include hematuria and renal colic from oxalate calculi, UTI and pyuria, hypertension, and renal tubular acidosis.

Treatment involves correcting the underlying cause if possible. High-oxalate foods should be avoided, and fluid intake should be increased to increase urinary volume. Other interventions may include Ca carbonate (1 g po once/day to qid) to bind gut oxalate; pyridoxine supplements (3 to 3.5 mg/kg po once/day) to promote conversion of glyoxalate to glycine rather than to oxalate; neutral phosphate (orthophosphate—10 to 13 mg/kg tid) to increase the urinary excretion of pyrophosphate, an inhibitor of Ca precipitation (the extra oral phosphate can also modestly reduce urinary Ca excretion by binding dietary Ca in the intestinal lumen); K citrate (10 to 20 mEq tid with meals) to increase urinary Ca oxalate solubility; or thiazide diuretics to reduce urinary Ca excretion. Treatment when end-stage renal disease occurs due to an inherited disorder is combined liver and kidney transplantation.

Hypercalcemia: Hypercalcemia causes nephropathy by 2 mechanisms. Severe (> 12 mg/dL) temporary hypercalcemia may cause reversible renal insufficiency by renal vasoconstriction and natriuresis-in-duced volume depletion. Long-standing hypercalcemia and hypercalciuria lead to CTIN with calcification and necrosis of tubular cells, interstitial fibrosis, and calcification (nephro-calcinosis). Diagnosis is based on presence of hypercalcemia and unexplained renal insufficiency; nephrocalcinosis can be detected by ultrasonography or noncontrast CT. Treatment is management of hypercalcemia. Nephrolithiasis, renal tubular acidosis, and nephrogenic diabetes insipidus are common associated findings.

Chronic hypokalemia: Chronic hypokalemia of a moderate to severe degree may produce nephropathy with impaired urinary concentration and vacuolation of proximal tubular cells and occasionally of distal tubular cells. Chronic interstitial inflammatory changes, fibrosis, and renal cysts have been found in renal biopsies of patients with hypokalemia of > 1 mo. Treatment consists of correction of underlying causes and oral K supplements. Although the hypokalemia as well as the number and size of the cysts is reversible, the CTIN and renal insufficiency may be irreversible.

Heavy Metal Nephropathy

Lead: CTIN results as lead accumulates in proximal tubular cells. Short-term lead exposure causes proximal tubular dysfunction, including decreased urate secretion and hyperuricemia (the substrate for saturnine gout), aminoaciduria, and renal glucosuria. Chronic lead exposure (5 to 30 yr) causes progressive tubular atrophy, interstitial fibrosis, hypertension, and gout. Chronic low-level exposure may cause renal insufficiency and hypertension independent of tubulointerstitial disease. Children exposed to lead paint dust or chips, welders, battery workers, and drinkers of moonshine alcohol are most at risk. Diagnosis is usually made by whole blood lead levels. Alternatively, x-ray fluorescence may be used to detect increased bone lead concentrations, which reflect high cumulative lead exposure. Treatment with chelation therapy can stabilize renal function, but recovery may be incomplete.

Cadmium: Cadmium from contaminated water, food, and tobacco and from workplace exposures can cause nephropathy. Early manifestations are those of tubular dysfunction, including low mol wt tubular proteinuria (eg, 2 -microglobulin), aminoaciduria, and renal glucosuria. Symptoms and signs, when they occur, are attributable to chronic renal insufficiency and failure. Renal disease follows a dose-response curve. Diagnosis is suggested by a history of occupational exposure, increased levels of urinary-microglobulin, and increased urinary cadmium levels (> 7 ug/g creatinine). Treatment is elimination of cadmium exposure; chelation with Na calcium edetate (EDTA) may increase cadmium nephrotoxicity. Tubular proteinuria usually is irreversible.

Other heavy metals: Those that are nephrotoxic include copper, gold, uranium, arsenic, iron, mercury, bismuth, and chromium. All cause tubular damage and dysfunction (eg, tubular proteinuria, aminoaciduria) as well as tubular necrosis, but glomerulopathies may predominate with some compounds (mercury, gold). Treatment involves removal of the patient from further exposure and chelating agents (copper, arsenic, bismuth) or dialysis (chromium, arsenic, bismuth).

Reflux nephropathy is renal scarring induced by vesicoureteral reflux of infected urine into the renal parenchyma.

Chronic pyelonephritis also may play a role, but UTI without intrarenal reflux is unlikely to cause nephropathy. Vesicoureteral reflux (VUR) affects about 1 % of newborns and 30 to 45% of young children with a UTI; it is present in almost all children with renal scars and, for unknown reasons, is less common in black children. Children with gross reflux (up to the renal pelvis plus ureteral dilatation) are at highest risk of scarring.

Reflux requires incompetent ureterovesical valves or mechanical obstruction in the lower urinary tract. Young children with concave papillary tips are most susceptible because the papillary collecting duct orifices are normally wide open at the upper and lower poles; normal growth usually results in spontaneous cessation of intrarenal and vesicoureteral reflux by age 5. New scars in children > 5 yr are unusual but may occur after acute pyelonephritis.

Few symptoms and signs are present in young children, and the diagnosis is often overlooked until adolescence, when patients present with proteinuria, hypertension, and/ or renal insufficiency.

Diagnosis and staging of reflux is made by a voiding cystourethrogram (VCUG), which can demonstrate the degree of ureteral dilatation; radionuclide cystography can be used to diagnose but not to stage the condition. Renal scarring is diagnosed with 99m-techne-tium dimercaptosuccinic acid (DMSA) radionuclide scanning or with IVU, which is less sensitive. In older children in whom reflux is no longer active, a VCUG may not show reflux, although the DMSA scan shows scarring; cystoscopy can demonstrate evidence of previous reflux at ureteral orifices. Renal biopsy at this late stage shows CTIN and focal glomerulosclerosis, the cause of mild (1 to 1.5 g/day) to nephrotic range proteinuria.

Many children require no treatment. Children with low-grade reflux are usually given antibiotics because they are at low risk of developing severe renal disease. However, drug therapy is associated with a higher incidence of new episodes of acute pyelonephritis; incidence of new renal scars is similar in surgical and drug treatment groups. Patients with severe reflux can be given antibiotic prophylaxis or undergo surgical interventions, including ureteral reimplantation or endoscopic injection of materials behind the ureter to prevent reflux (bladder contraction during voiding compresses the ureter between the bladder and the material).

Reflux spontaneously resolves in about 80% of young children within 5 yr. Persistent VUR may cause slowly progressive renal failure.


Myeloma-Related Kidney Disease

Patients with multiple myeloma overproduce monoclonal Ig light chains (Bence Jones proteins); these light chains are filtered by glomeruli, are nephrotoxic, and can damage virtually all areas of the kidney parenchyma.

The mechanisms of nephrotoxicity are unknown. Tubulointerstitial and glomerular damage are most common.

Tubulointerstitial disease: Light chains saturate the reabsorptive capacity of the proximal tubule, reach the distal nephron, and combine with filtered proteins and Tamm-Horsfall mucoprotein (secreted by the thick ascending limb cells) to form obstructive casts. The term myeloma kidney generally refers to renal insufficiency caused by the tubulointerstitial damage that results. Factors that predispose to cast formation include low urine flow, elevation of luminal NaCl concentration (eg, due to a loop diuretic), radiocontrast agents, and increased intratubular Ca from the hypercalcemia frequently occurring from bone lysis in multiple myeloma.

Other types of tubulointerstitial lesions associated with Bence Jones proteinuria include proximal tubular transport dysfunction producing Fanconi syndrome and light chain interstitial deposition with inflammatory infiltrates and active tubular damage.

Glomerulopathies: Myeloma glomerulopathy has 2 common mechanisms: AL amyloidosis and glomerular light chain deposition. AL amyloidosis results in mesangial and/or subepithelial glomerular deposition of AL amyloid, randomly oriented, nonbranching fibrils composed of the variable regions of X light chains. Light chain deposition disease (LCDD), which also can occur with lymphoma and Waldenstrom's macroglobulinemia, is glomerular deposition of nonpolymerized light chains, generally the constant regions of K chains.

Less commonly, a nonproliferative, noninflammatory glomerulopathy that causes nephrotic range proteinuria can develop in advanced myeloma-related renal disease, and a proliferative glomerulonephritis occasionally develops as an early form of LCDD with progression to membranoproliferative glomerulonephritis and nodular glomerulopathy reminiscent of diabetic nephropathy.


Symptoms, Signs, and Diagnosis

Symptoms and signs are predominantly those of the myeloma (skeletal pain, pathologic fractures, diffuse osteoporosis) and a normochromic-normocytic anemia.

Diagnosis of myeloma-related kidney disease is suggested by findings of renal insufficiency, usually accompanied by bland urine sediment and a negative or trace-positive dipstick for protein (unless urine albumin is elevated in a patient with an accompanying nephrotic syndrome). Diagnosis of light chain tubulointerstitial disease is confirmed by a markedly positive urine sulfosalicylic acid test suggesting significant nonalbumin proteins and/or urine protein electrophoresis (UPEP). Diagnosis of glomerulopathy is confirmed by renal biopsy. Renal biopsy may demonstrate light chain deposition in 30 to 50% of patients despite the absence of detectable serum or urine paraproteins by immuno-electrophoresis.

Prognosis and Treatment

Prognosis is good for patients with tubulointerstitial and glomerular LCDD who receive treatment. Prognosis is worse for patients with AL amyloidosis, in whom amyloid deposition continues and progresses to renal failure in most cases. In either form without treatment, virtually all renal lesions progress to renal failure.

Treatment is management of multiple myeloma combined with prevention of volume depletion and maintenance of a high urine flow rate. Alkalinization of the urine helps change the net charge of the light chain and reduces charge interaction with Tamm-Horsfall mucoprotein, making the light chains more soluble. Colchicine decreases Tamm-Horsfall mucoprotein secretion into the lumen and decreases the interaction with light chains, thus decreasing toxicity. Avoidance of loop diuretics prevents volume depletion and high distal Na concentrations that can worsen myeloma-related kidney disease.


V. MATERIALS FOR METHODICAL MAINTENANCE


5.1. Control materials of a preparatory stage of the lesson


5.1.1. Theoretical question to the lesson:

  1. The mechanisms of occurrence of tubulointerstitial nephritis.

  2. Pathogenesis of various types of tubulointerstitial nephritis.

  3. Causes of acute tubulointerstitial nephritis.

  4. Causes of cronic tubulointerstitial nephritis.

  5. Classification of tubulointerstitial nephritis.

  6. Data additional laboratory and instrumental methods of diagnostics.

  7. Differential diagnosis of different types of tubulointerstitial nephritis.

  8. Principles of treatment of different types of tubulointerstitial nephritis.

  9. Indications for surgical treatment of patients with this pathology.
5.1.2. Practical tasks to the lesson:

  1. To be able to make inquiry of compleints and to make the anamnesis of patients with tubulointerstitial nephritis

  2. To be able to make the objective examination of patients with tubulointerstitial nephritis.

  3. To be able to formulate the preliminary diagnosis.

  4. To be able to make the plan of inspection of the patient.

  5. To be able to realize the differential diagnosis of patients with tubulointerstitial nephritis.

  6. To be able to prove drug treatment of the patient.

5.2. Materials for the control of the final stage of the lesson:


1. The patient of 32 years has arrived with complaints per a fever, rise in temperature to 38C, pains in the lumbar area, frequent urination. In the analysis of urine leukocytes are – 15 - 20 per HPF, erythrocytes – 3 – 4 per HPF. protein – 0,52 g/l, bacteria – 10 /ml It is the most reasonably to appoint:

  1. Norfloxacin

  2. Oxacillin

  3. Penicillin

  4. Streptomycin

  5. Sulfadimine
2. The woman with term of pregnancy of 18 weeks is hospitalised to the urological hospital because of occasion of a acute right-hand pyelonephritis. Urine outflow is restored by means of "stent" statement. Which antibacterial means should be appointed?

  1. Aminoglycosides and/or fluoroquinolones

  2. Macrolides and/or tetracyclines

  3. Aminoglycosides and/or macrolides

  4. Polymyxin and/or rifampicin

  5. Penicillins and/or cephalosporins
3. The patient of 37 years, female, complains of a dull pain in the left lumbar area which periodically amplifies, rise in temperature of a body to 38,7, speeded up of urination. She is ill about 4 years, has arisen after considerable overcooling. Objectively: pulse - 80 per minute, rhythmical, the arterial pressure - 160/100 mm hg. Fin heart and lungs deviations from norm it is not revealed. Tenderness is marked at palpitation of both kidneys, more at the left, in the same place a positive Pasternatsky's symptom. Edema are not present. The urine analysis: urine specific gravity – 1012, protein – 0,99g/l, leukocytes – 12 – 14 per HPF, erythrocytes – 2 – 3 per HPF. Erythrocyte sedimentation reaction – 22mm/h. Your diagnosis?

  1. Acute pyelonephritis

  2. Chronic glomerulonephritis

  3. Chronic pyelonephritis

  4. Renal colic

  5. Chronic cystitis

5. A 68-year-old woman presented to her GP. She was found to have symptoms and signs of active synovitis, with elevated inflammatory markers. She had been taking IM sodium aurothiomalate 50 mg once a week for the previous six months. Other medications included diclofenac 50 mg three times a day. She had well controlled ischaemic heart disease and recent onset atrial fibrillation. Her medications also included aspirin 75 mg, recently changed to warfarin. Her renal function, meas­ured a month previously, had been normal.

Recent investigations revealed:

serum sodium 138 mmol/L

serum potassium 4.9 mmol/L

serum urea 12.9 mmol/L

serum creatinine 290 umol/L

Urinalysis: protein (++), blood (++)

24-hour urine collection: 0.4 g protein/day

What is the most likely cause for her deterioration in renal function?

B. gold nephropathy

C. interstitial nephritis

D. multiple myeloma


  1. Mark H. Beers, Robert S. Porter, Thomas V. Jones, Justin Kaplan, Michael Berkwits The Merk Manual of Diagnosis and Therapy/ Merk Research Laboratoris, 2006, P. 2015-2023.

  2. Fedosyeva V.M. Khrenov A.A. Therapy. The course of lectures. /Simferopol, - 2003, - P. 405-422.

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PPT - Tubulointerstitial Disease PowerPoint Presentation

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Aims & objectives
  • State the definition of tubulointerstitial disease.
  • Identify clinical signs of tubulointerstitial disease.

  • Explain the pathophysiology of tubulointerstitial disease.

    TubulointerstitialNephrithis

    The tubulointerstitial compartment is affected in all the forms of renal disease. We can findthepathology astubular damage, tubular atrophy, edema, interstitial inflammationor fibrosis.

    Acute interstitial or tubular damage can produce acute renal failure,

    Chronicchanges are a good indicator of irreversible lesions primary injury to renal tubules and interstitium resulting decreased renal function.

    AcuteTubulointerstitialNephrithis

    The acute form is most often due to allergic drug reactions or to infections.

    suggested by history and urine and blood tests and confirmed by biopsy.

    Exclusion of glomerular disease

    Urinalysis: proteinuria<1 g/day (Proteinuria is usually minimal but may reach nephrotic range with combined ATIN-glomerular disease induced by NSAIDs)

    WBC casts and granular casts

    Low molecular weight proteinuria (LMW-P)

    ( B2 micglobulin, Tamm-Horsfall gylcoprotein)

    Diagnosis of ATIN

    Tamm-Horsfall gylcoprotein
    • The most abundant protein of renal origin
  • Synthesized by cells of the thick ascending limb of the loop of Henle

  • Excreted in the urine at a relatively constant rate

  • Urinary excretion can increase following injury to the distal tubule

    Diagnosis of ATIN
    • Eosinophiluria has a positivepredictivevalue of 50% and a negativepredictivevalue of 90% for ATIN; absencesignificantlyexcludesdisease.

    Blood test findings of tubulardysfunctioninclude;

  • hyperkalemia (defect in K excretion)

  • metabolicacidosis(defect in acidexcretion)

    Ultrasoundfindings:Thekidneysmay be greatlyenlargedandechogenicbyexaminationbecause of interstitialinflammatorycellsandedema.

    Renalbiopsy
    • not often performed for diagnostic purposes but has helped characterize the nature and progression of tubulointerstitial disease.
  • Glomeruli are usually normal. The earliest finding is interstitial edema, typically followed by interstitial infiltration with lymphocytes, plasma cells, eosinophils, and a few PMNs.

  • The presence of granulomas suggests sarcoidosis.

    Acute Tubulointerstitial Nephritis

  • Test: Renal

    5 Written questions
    1. THIAZIDE DIURETIC. INHIBITS NaCl REABSORPTION IN EARLY DISTAL TUBULE!

    DECREASES Ca EXCRETION (increases reabsorption in PCT!)

    USES: HTN, CHF, HYPERCALCIURIA, NEPHROGENIC DIABETES INSIPIDUS, KIDNEY STONES

    Toxicity HYPER: GLYCEMIA, LIPIDEMIA, URICEMIA, CALCEMIA.
    Also; Hypokalemia and hyponatremia
  • HYPOALDOSTERONISM or lack of collecting tubule response to aldosterone. Associated with INCREASED K+ and inhibition of NH4 excretion in PCT.
    PRINCIPAL CELL Na CHANNEL DEFECT

    LOW URINE pH due to decreased buffering capacity. NO KIDNEY STONES!

    causes:
    Diabetes
    Urinary obstruction, Medications (Bactrim, K-sparing diuretics), Renal interstitial inflammation
  • Afferent Arteriole winds through the glomerulus --> Efferent Arteriole. Filtrate from the glomerulus --> to the PCT in the cortex --> descending limb in the medulla --> up the ascending limb --> DCT in the cortex --> Collecting duct (which runs parallel to the vasa rect so it can reabsorb any materials from the collecting duct.

  • Additive to milk formulas, many children in China were hospitalized from it and some died.

  • Dilation of Calyces = Caliectasis
    HYDRONEPHROSIS = SWELLING OF URINARY TRACT BEHIND OBSTRUCTION
  • 5 Matching questions
    1. Lower Urinary Tract Obstruction (LUTO) ±
    2. Maintenance phase of Alkalosis
    3. PODOCYTE LAYER AS A BARRIER
    4. Acute Tubular Necrosis General
    5. Acute TIN - Urinalysis
    1. a
      Reflux, Hydronephrosis with Hydroureter
    2. b Persistent hyperaldosterone state / continued acid loss or alkali therapy


      CHLORIDE DEPLETION --> Bicarbonate RETENTION!
      H+ loss in Type A intercalated cells
      Alkali retention in Type B cells

      Remember: Aldosterone --> Na reabsorption in exchange for K+, H+ will also be secreted into the negative lumen by the intercalated cells.
    3. c MCC of Acute Renal Failure in hospital!

      Death may (and most often) occurs during initial oliguric phase.

      Associated with renal ischemia (shock / sepsis), crush injury, toxins.

      LOOK FOR MUDDY BROWN CASTS
    4. d Gross hematuria 5-20%
      Micro-hematuria 70-90%
      Proteinuria (1-2 Gm/day) 70-85%
      Pyuria 70-80%
      FENa > 1% 100%
    5. e The "charge" barrier: the podocytes are also coated in negatively charged proteins.

      The "size" barrier: the slit diaphragm consists of interlocking proteins that form a zipper with intervening pores that are just small enough to prevent most proteins from escaping through them

    5 Multiple choice questions
    1. Prevention:
      AVOID HYPOTONIC SOLUTIONS in Post-Op patients!

    Consider prophylactic INTUBATION in young FEMALES with HYPONATREMIA and impending encephalopathy

    Tx for CHRONIC HYPONATREMIA: NORMAL SALINE

    Tx for SYMPTOMATIC HYPONATREMIA: Saline initially, if hypovolemia existed
    Re-evaluate
    3% NaCl + diuretics in euvolemic patients

    Do not exceed 12meq/24 hours!
    Do not exceed 18 meq/48h DON'T OVER CORRECT!
    1. Treatment of hyponatremia
    2. Melamine Milk Crisis
    3. ATN pathogenesis
    4. Treatment of Metabolic Alkalosis

  • Common:
    Acyclovir
    HAART (e.g. indinavir, atazanavir)
    1. Creatinine
    2. Calcitonin
    3. Aldosterone
    4. Drug Stones
  • Pumps transport compounds from the plasma into the lumen of the nephron
    Two kinds of "pumps":
    For organic acids (uric acid, p-aminohippuric acid, diuretics, antibiotics, etc. )
    For organic bases (creatinine, procainamide, choline, etc. )
    Pumps are located in the proximal tubule
    1. Active Tubular Secretion
    2. Diffuse Cortical Necrosis
    3. Transplant rejection
    4. Clearance

  • Most patients managed by General Medicine
    Stage I-IV handled by Generalists (PCP)
    Stages IV & V managed by Renal PCP Gross Changes: Bilateral contracted kidneys
    Thin renal Cortex
    Multiple cysts (acquired cystic disease) ^
    1. Causes of Edema
    2. Drug Storage Site -
    3. Handling Stages of CKD
    4. Hyaline Casts
  • DM Ketoacidosis
    Insulin deficiency AND any stress like infection, MI etc
    Dipstick picks up ONLY acetoacetate (not BetaOH-B)
    Bicarbonate used only with severe acidemia
    Ketones are "potential" bicarbonate Alcoholic ketoacidosis
    Predominantly BetaOH-B: not strongly (+) on dipstick
    HYPOGLYCEMIA, INSULIN LOW
    Treatment: VOLUME REPLACEMENT WITH SALINE and GLUCOSE
    1. Drug Stones
    2. Kidney Stones
    3. Ethacrynic Acid
    4. Ketoacidosis
  • 5 True/False questions

    Functional Adaptations in GFR → Reduction in functioning nephrons will lead to an increase in systemic hypertension and increase in SNGFR (single nephron glomerular filtration rate)
    Compensatory 'functional' mechanism

    Leukocyte esterase and Nitrites in Urinalysis → The addition of ACE inhibitors in the presence of bilateral (not unilateral) RAS will cause kidney failure.

    The efferent arteriole is mostly dependent on angiotensin-II for its vascular tone. By dilating it you decrease GFR to almost --> 0. --> Destruction of the nephrons (they must filter to survive!).

    MINIMAL CHANGE DISEASE Treatment and Prognosis → Sloughing off of Renal Papilla --> Gross hematuria, proteinuria. May be caused by RECENT INFECTION

    Associated with:
    1. DM
    2. Acute Pyelonephritis
    3. Chronic Phenacetin use (acetominophen)
    4. Sickle Cell Anemia

    THERAPEUTIC IMPLICATIONS of Glomerular Disease → Plasmapheresis: Elimination of circulating pathogenetic antibodies

    Immunosuppression: Against T cell functions, B cell functions, complement activation, antigen-antibody formation

    Pharmacologic inhibitions of mediator molecules

    IF pics and EM of different diseases → AUTOSOMAL RECESSIVE inheritance.
    Predominately INFNATS. but
    Rare, affects 1 in 20,000 - 50,000 individuals
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    High mortality if early ESRD in childhood.

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    Top 10 deadliest diseases

    Top 10 deadliest diseases

    Ever since the inception of human race, diseases have claimed lives more than anything else in the world — be it a natural calamity, war or anything else. However, science have championed a lot in current time, yet there are plethora of diseases that have no remedy till the date. From the stack of curable and non-curable ones, this page examines top 10 deadliest diseases that have terrified the masses staggeringly.

    10. Tetanus:

    Tetanus, sometimes known as lockjaw, is a disease manifested by uncontrolled muscle spasms. The disease is frequently fatal, especially to the very old or very young, and is preventable by immunization. Fortunately, most children are immunized for tetanus at the same time they receive the vaccine for Diptheria .

    9. Diarrhea:

    The most common cause of diarrhea is a virus that infects the gut. The infection usually lasts for two days and is sometimes called “intestinal flu” or “stomach flu”. The pediatric death toll due to diarrheal illnesses exceeds that of AIDS, tuberculosis, and malaria combined. In poor countries, diarrheal disease is second only to pneumonia in causing the deaths of children under five years old.

    8. Smallpox:

    Smallpox is a serious, contagious, and sometimes fatal infectious disease. There is no specific treatment for smallpox disease, and the only prevention is vaccination. The name smallpox is derived from the Latin word for “spotted” and refers to the raised bumps that appear on the face and body of an infected person. It spreads through tiny drops of an infected person’s saliva (spit) when the person coughs, talks, or sneezes. Smallpox usually passes from person to person during close, face-to-face contact.

    7. Plague:

    Generated by rodents, Plague is one of the most deadliest diseases which has claimed several lives throughout its existence of more than 2,000 years. Basically there are three types of plague — bubonic plague, pneumonic plague and septicemic plague. Along with rats, fleas are also associated with this diseases which attacks person depending on sanitary conditions or by direct contact.

    6. Cancer:

    Cancer is a class of diseases characterized by out-of-control cell growth. There are over 100 different types of cancer, and each is classified by the type of cell that is initially affected. One of the most insidious aspects of cancer is the way it grows. As the tumor outgrows the original organ, pieces of malignant tissue often break off (metastasize) and enter the bloodstream or lymph system.

    5. Cholera:

    Cholera is a serious infectious disease caused by the bacteria Vibrio Cholerae, which affects the intestinal system of the body. An infected person experiences severe vomiting, explosive diarrhea and severe dehydration. Without immediate medical treatment, cholera may result in death within four to twelve hours after symptoms begin. Due to a large loss of body fluids, cholera is gruesome in the way that it leaves survivors in their physical appearance, as well as in the biological toll it takes on the body.

    4. Tuberculosis:

    Tuberculosis (TB) is a common and often deadly infectious disease caused by mycobacteria, usually ”Mycobacterium Tuberculosis” in humans. Tuberculosis usually attacks the lungs but can also affect other parts of the body. It is spread through the air, when people who have the disease cough, sneeze, or spit. Most infections in humans result in an asymptomatic, latent infection, and about one in ten latent infections eventually progresses to active disease, which, if left untreated, kills more than half of its victims.

    3. Malaria:

    Approximately 300 million people worldwide are affected by malaria and between 1 and 1.5 million people die from it every year. Previously extremely widespread, the malaria is now mainly confined to Africa, Asia and Latin America. There are more than 2,500 known species of mosquitoes worldwide. Out of that, only around 50 to 60 species of Anophelis mosquitoes are capable of transmitting the infection.

    2. AIDS:

    AIDS stands for Acquired immunodeficiency (or immune deficiency) Syndrome. One of the deadliest diseases with no remedy so far, AIDS results from infection with a virus called HIV, which stands for Human Immunodeficiency Virus. This virus infects key cells in the human body called CD4-positive (CD4+) T cells. These cells are part of the body’s immune system, which fights infections and various cancers. Being HIV-positive, or having HIV disease, is not the same as having AIDS. Many people are HIV-positive but don’t get sick for many years. As HIV disease continues, it slowly wears down the immune system. Viruses, parasites, fungi and bacteria that usually don’t cause any problems can make you very sick if your immune system is damaged. These are called “opportunistic infections”.

    1. Heart Disease:

    There are many kinds of heart diseases, and they can affect the heart in several ways. But the ultimate problem with all varieties of heart diseases is that, in one way or another, they can disrupt the vital pumping action of the heart. The most common form of heart disease is coronary heart disease, also known as coronary artery disease (CAD).

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