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An Unusual Case Of Renal Failure

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  • 1. AN UNUSUAL CASE OF RENAL FAILURE Dr.P.ARUL. PG Prof. VIJAYARAGAVAN’s Unit
  • 2. 60 years old female patient Sabira admitted with complaints of Burning micturition For 3 days Abdomen pain Fever
  • 3. H/o Presenting illness : Fever – High grade, intermittent , associated with chills. Abdomen pain – Lower abdomen and also in the flanks. Burning micturition+ No C/o vomiting. No C/o oliguria. No C/o Facial puffiness or leg swelling.
  • 4.
    • Past History
    • DM – 3 years
    • HT – 6 months
    • Personal History – Not a smoker or alcoholic or tobacco chewer.
    • Family History – No H/o similar illness.
    • Contact History – No H/o contact with tuberculous patients.
    • Drug History – No H/o ingestion of NSADS.
  • 5.
    • General Examination
    • Pt conscious
    • Oriented
    • Afebrile
    • Anemic
    • Not jaundiced
    • No cyanosis
    • No clubbing
    • Pedal edema+
    • No generalised lymphadenopathy
  • 6.
    • Vital Parameters
    • BP 130 /80
    • Temp 98.4 F
    • Pulse 80/min
    • RR 18/min
  • 7.
    • Systemic examination
    • CVS – S 1 S 2 + No murmur.
    • RS – NVBS, No added sounds.
    • PA - Soft, No organomegaly, suprapubic tenderness+.
    • CNS – No FND.
  • 8. Investigations
    • CBC
    • WBC– 13.6 X 10 3 /ml. dc p61% l 38% e1%
    • RBC – 3.98 X 10 6 /ml
    • HB – 7.2 gm /dl
    • MCH – 18.1 pg
    • MCHC – 29.6 gm/l
    • PLT – 2.9 lacs
    • ECG - WNL
    • CHEST XRAY – normal
    • URINE – Sugar nil, alb-nil, dep – 1 to 2 puscells
  • 9.
    • 28/9 5/10 8/10 10/10 25/10
    • Blood Sugar – F 131 90 94 102 86
    • PP 207 101 150 132 117
    • Urea 150 88 79 80 101
    • Creatinine 7.6 2.3 2.4 2.0 2.1
    • Sodium 138 135 135 136 138
    • Potassium 4.1 4.0 3.8 4.1 4.2
    • Calcium 7.8
    • Phosphorus 4.6
    • Uric Acid 5.9
    • 24 hrs U Protein 90 mg/l
    • Volume 1500 ml
  • 10.
    • U/S abdomen – small left kidney, RT – hydro uretero nephrosis.
    • RK – 11 x 6.4 cms PCS dilated upper and middle ureter measures 7 mm
    • LK – normal PCS 7.7 x 3.5 cms
    • CT abdomen – bilateral hydro nephrosis with small left kidney.
    • Urine C/s – 3/09/09 klebsiella grown, HS cefotaxime, amikacin
    • 9/10/09 klebsiella grown, HS amikacin
  • 11.
    • DIAGNOSIS – DM/SHT/UTI/CKD non oliguric/ anemia
    • TREATMENT –
    • Pt treated with cefotaxime, metronidazole, lasix and insulin.
    • Pt taken over by nephrologist.
    • HD done.
    • On 16/10/09 for RT – HUN DJ stent done by urologist.
  • 12. DISCUSSION
  • 13. DIABETES &KIDNEY RELATED COMPLICATIONS
    • DIABETIC NEPHROPATHY
    • Glomerulonephritis
    • Membranous nephropathy
    • Renal papillary necrosis
    • Renovascular disease
    • Autonomic neuropathy of bladder
    • UTI – Acute pyelonephritis
    • Renal tuberculosis
    • Contrast nephropathy
  • 14. Renal dysfunction in DM
    • Stage I
      • Renal hypertrophy and hyperfilteration
      • UAER, GFR & RPF increased
    • Stage II
      • GFR increased
      • UAER & BP normal
      • BM thickening
      • Increased mesangial volume
    • Stage III
      • Microalbuminuria or incipient nephropathy
      • GFR normal or increased
      • UAER 30-300mg/24hrs
      • BP increased
      • Increased BM thickening and fractional mesangial volume within the glomeruli
      • Subsequently decrease in GFR
  • 15.
    • Stage IV
      • Overt nephropathy
      • HT, proteinuria
      • NS is common
      • GFR decreased
    • Stage V
      • ESRD
      • Median survival of 7yrs from the development of persistent proteinuria if no intervention undertaken
  • 16. Renal pathology in DM
    • Size
      • Larger & wt increase an average of 15%
      • Increase in protein & RNA content
      • Increase in DNA synthesis
      • Renal size increased till ESRD is established
      • Renal hypertrophy may be due to compensatory growth in the face of glomerular loss
      • PAS staining material get filled up in atropic ischemic glomeruli
      • In DM renal volume continues to increase as UAER rises to the level of overt proteinuria
  • 17. UAER
    • ACR >2 predicts UAER >30/ µg/min
    • Cut off for ACR in
      • Male >2.5
      • Female >3.5
    >200 >300 Overt nephropathy 20-200 30-300 Microalbuminuria <20 <30 Normoalbuminuria overnight 24hrs(mg/day)
  • 18. Renal papillary necrosis
    • Renal papillary necrosis (RPN) is characterized by coagulative necrosis of the renal medullary pyramids and papillae
    • Renal papillary necrosis generally affects individuals who are in the middle decades of life or older
    • It is more common in women than in men
    • 60% of the patients have DM, 30% Urinary tract obsruction, 15% have both.
    • Renal papillary necrosis is primarily a bilateral process
  • 19. Etiology
    • Pyelonephritis
    • Obstruction of the urinary tract
    • Sickle cell hemoglobinopathies, including sickle cell trait
    • Tuberculosis
    • Cirrhosis of the liver, chronic alcoholism
    • Analgesic abuse
    • Renal transplant rejection, Radiation, Renal vein thrombosis
    • Diabetes mellitus
    • Systemic vasculitis
  • 20. Analgesic induced RPN
    • One of the most common and most preventable etiologic factors is the use of analgesics.
    • In healthy individuals in whom renal arterial blood flow is not compromised, NSAIDs have little effect unless they are used in excess.
    • The normal kidney is not relying on the vasodilatory effects of prostaglandin to supply adequate perfusion. However, in patients who are predisposed to renal hypoperfusion, local prostaglandin synthesis protects the glomeruli and tubules from ischemia. The inhibition of prostaglandin synthesis by NSAIDs that inhibit COX-1 and COX-2, removes this protective mechanism and predisposes the kidney to further renal hypoperfusion and, ultimately, ischemia.
    • Additionally, a short course of NSAIDs has caused papillary necrosis and nonoliguric renal failure in otherwise healthy individuals as young as age 17 years. A case such as this may be an anomaly, but caution is warranted when prescribing NSAIDs, and adequate hydration is recommended.
  • 21. Pathophysiology
    • Renal papillary necrosis is classified depending primarily on the patient's degree of impaired vasculature as
      • Focal (ie, involving only the tip of the papilla) or
      • Diffuse (ie, involving the whole papilla and areas of the medulla)
    • Researchers recognize 2 pathologic forms of renal papillary necrosis—the medullary form and the papillary form .
    • Patients with medullary ischemia develop decreased glomerular filtration rates, salt wasting, an impaired ability to concentrate, and polyuria because the vasa rectae supply the medulla and serve the countercurrent exchange mechanism.
  • 22. Normal kidney Hypoperfused kidney Does not depend upon local Prostaglandins for adequate perfusion Depend upon local Prostaglandins for adequate perfusion NO EFFRECT RENAL PAPILLARY NECROSIS ANALGESICS – COX1/COX2 INHIBITORS
  • 23. Presentation
    • Renal papillary necrosis has a variable clinical course that ranges from a chronic, protracted, and relapsing form to an acute, rapidly progressive form.
    • The acute progressive form is particularly rare, but the effects are devastating, resulting in death from septicemia and renal failure, requiring dialysis and potentially resulting in death.
    • Patients with the more common chronic form may remain asymptomatic until diagnosed incidentally.
    • The most common presenting symptoms in symptomatic patients include fever and chills, flank and/or abdominal pain, and hematuria.
    • Acute renal failure with oliguria or anuria is rare; when these symptoms develop, the disease may be fulminant, If renal function deteriorates suddenly in a patient with confirmed diabetes or in a patient with a known history of chronic obstruction and/or pyelonephritis, consider the diagnosis of papillary necrosis, even if the patient is asymptomatic.
  • 24. Diagnosis
    • CT findings include
      • (1) small kidneys,
      • (2) ring shadows in the medullae,
      • (3) contrast-filled clefts in the renal parenchyma,
      • (4) renal pelvic filling defects.
    • IVU findings include
      • (1) shrinkage and irregularity of papillae,
      • (2) desquamated papilla in situ, demarcated by contrast material as a ring shadow (commonly referred to as the ring sign);
      • (3) a calix without a papilla;
      • (4) a partially calcified filling defect in the renal pelvis
      • (5) contrast-containing rice-grain–sized cavities in the papilla, which are pathognomonic for the medullary form of renal papillary necrosis.
    • Ultrasonography findings may suggest the diagnosis late in the course of the disease but is not sensitive enough to be confirmatory in the earlier.
  • 25. Excretory urography in a patient with renal papillary necrosis and pyeloureteritis cystica. There is bilateral loss of the renal mantle with contrast tracking from the renal fornix in the lower pole of the right kidney. There is also multiple smooth filling defects in the ureter, caused by ureteritis cystica
  • 26. Photograph of a gross section from the right kidney shows abscesses in the cortex (arrowheads) and hemorrhagic infarcts in papillary regions (arrows), findings indicative of pyonephrosis and necrotizing papillitis, respectively.
  • 27. Treatment
    • Medical
      • Acute disease may require broad-spectrum intravenous antibiotics, hydration, glycemic control, and urinary alkalinization. Cessation of analgesic.
      • Patients with sickle cell disease may require exchange transfusions
    • Surgical
      • Acute obstruction with concomitant urinary tract infection is a urologic emergency that requires immediate percutaneous nephrostomy to relieve the obstruction, ureteral stent placement, or endoscopic retrieval of the obstructing sloughed papillae
      • Nephrectomy may be life-saving in patients with overwhelming infection
  • 28. Other renal diseases in DM
    • Glomerulonephritis
      • Every form of glomerular disease reported
      • Membranous nephropathy most commonly
    • Renal papillary necrosis
      • More common in female
      • Can be asymptomatic
      • Microscopic hematuria is frequent & sterile pyuria is typical
      • Modest proteinuria is common
    • Renovascular disease
      • Increased incidence
      • Increased frequwncy in association with PVD
      • HT is common
  • 29.
    • UTI
      • Asymptomatic bacteruria in women
      • Increase in symptomatic UTI in pregnancy
    • Acute pyelonephritis
      • Leads to perinephric abcess
      • Urine culture may be negative with fever & flank tenderness
      • Gram – ve organism common
      • 90% of cases of emphysematous pyelonephritis occur in pt. with DM
    • Renal tuberculosis
      • Increased risk of developing renal tuberculosis
    • Contrast nephropathy
      • Increased rise of renal deterioration of renal function following use of contrast media
  • 30. Autonomic neuropathy of bladder
    • Prevalence is 40% in long standing diabetes
    Functional incompetence of UV junction Recurrent UTI Urethral sphincter dysynergy Weakened bladder contraction & incomplete emptying. Increased residual volume Noctuira Decrease in daytime micturition frequency Disruption of parasympathetic innervation to detrusor & efferent sympathetic innervations to trigone Decreased awareness of bladder distension & then micturition at progressively larger volumes Asymptomatic Destruction of proprioceptive afferent fibres Sign Symptoms Pathology
  • 31. Thank you
  • 32. 9 0 At diagnosis 15 15 Overt nephropathy 38 16 Microalbuminuria Type 2 DM Type 1 DM Prevalence
  • 33. Investigation & treatment for microalbuminuria
    • Monitor serum creatinine
    • Check retinopathy
    • Investigate other causes of renal pathology
    • Screen for IHD & PVD
    • Screen & treat HT aggressively
    • Assess lipid profile
    • Discourage smoking
    • Tighten glycemic control
  • 34. Albuminuria in type 1 DM and development of complications 50 11 58 80 Macroalbuminuria 31 6 28 40 Microalbuminuria 21 1 12 20 Normoalbuminuria Prevalence of neuropathy % Prevalence of blindness % Prevalence of retinopathy % Prevalence of HT % UAER
  • 35. Diabetic nephropathy
    • Characterized by persistent albuminuria >300mg/24hrs or >200 μ g/min on at least 2 occasions separated by 3-6 months
    • Since type 2 DM is 10-15 times more common than type 1 DM, the prevalence of type 2 diabetic nephropathy is substantially higher
    • Gender:
      • M:F in type 1 DM 1.7:1
      • In type 2 DM 5:1
    • Age at onset of DM :
      • Puberty – disproportionate increase in renal hypertrophy during the phase of puberty has been noted recently
      • >50yrs – high prevalence of microalbuminuria than those diagnosed before the age of 40yrs
  • 36. Indications for renal biopsy
    • Renal biopsy should be considered
      • In the absence of retinopathy
      • With sudden & rapid onset of proteinuria (particularly if disease duration is less than 5yrs)
      • Abnormal evolution without transition through usual stages eg. The development of NS wothout previous microalbuminuria

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