1. Chronic Kidney Disease:Chronic Kidney Disease:
Diagnosis and managementDiagnosis and management
Dr Vilas Naik,Dr Vilas Naik, Consultant NephrologistConsultant Nephrologist
Kolhapur Kidney Care and Superspeciality Centre,Kolhapur Kidney Care and Superspeciality Centre,
VijayVijay HospitalHospital,, KolhapurKolhapur
IMA Ratnagiri
4th
July 2009
2. OverviewOverview
CaseCase
DefinitionDefinition
Epidemiology: Indian ScenarioEpidemiology: Indian Scenario
Risk Factors and CausesRisk Factors and Causes
How do we suspect?: Clinical features andHow do we suspect?: Clinical features and
complicationscomplications
DiagnosisDiagnosis
Management and Slowing the progression of KidneyManagement and Slowing the progression of Kidney
DiseaseDisease
3. CaseCase
36 yrs young lady36 yrs young lady
2 kids, No pregnancy complications2 kids, No pregnancy complications
Presenting illnessPresenting illness
– Generalized weakness & bone painsGeneralized weakness & bone pains
– dyspnea on exertiondyspnea on exertion
– decreased appetite since 6 monthsdecreased appetite since 6 months
– Wt loss by 2-3 kgsWt loss by 2-3 kgs
4. CaseCase
– Investigated 4 months ago:Investigated 4 months ago:
Weight: 34 kgs, ? Fever, BP- 150/ 96,Weight: 34 kgs, ? Fever, BP- 150/ 96,
Hb- 9.2 gm %,Hb- 9.2 gm %,
Bilirubin, SGOT and SGPT was normalBilirubin, SGOT and SGPT was normal
– Urine: albumin – 3+, RBCs- 12-15, WBCs- 10-12Urine: albumin – 3+, RBCs- 12-15, WBCs- 10-12
– Creatinine-Creatinine- 1.4 mg %1.4 mg % (lab range 0.5 to 1.4 mg%)(lab range 0.5 to 1.4 mg%)
– CXR- NormalCXR- Normal
5. CaseCase
– Treated with antibiotics for ? Fever, antimalarials,Treated with antibiotics for ? Fever, antimalarials,
then as UTI.then as UTI.
– She felt persistently unwell + weight loss: So wasShe felt persistently unwell + weight loss: So was
started on AKTstarted on AKT
– Presently: May 2009Presently: May 2009
HT: 160/96, Wt- 33 kgs, Nothing else on examinationHT: 160/96, Wt- 33 kgs, Nothing else on examination
Anemia: Hb: 8.8 gm%, Sr.Ca: 7.3 mg%Anemia: Hb: 8.8 gm%, Sr.Ca: 7.3 mg%
Urine: Albumin- 4+, RBCs- 3-4, Pus Cells- 6-8.Urine: Albumin- 4+, RBCs- 3-4, Pus Cells- 6-8.
SGOT, SGPT, Bilirubin- NormalSGOT, SGPT, Bilirubin- Normal
Creatinine:Creatinine: 2.4 mg%,2.4 mg%, USG – Kidney sizes 7.3 and 7.2 cmsUSG – Kidney sizes 7.3 and 7.2 cms
6. Case ContinuedCase Continued
Nephrology consulted for mild renal failureNephrology consulted for mild renal failure
Past Medical HistoryPast Medical History was evaluated inwas evaluated in
more detailmore detail
– Puffiness of face and mild edema feet – 1 yr agoPuffiness of face and mild edema feet – 1 yr ago
– was told to have slightly high BP, takenwas told to have slightly high BP, taken
amlodepin and lasix for 15 days.amlodepin and lasix for 15 days.
– Urine- albumin- 2+, RBCs- 8-10, Pus cells- 8-10.Urine- albumin- 2+, RBCs- 8-10, Pus cells- 8-10.
– CBC normal. Improved with symptomaticCBC normal. Improved with symptomatic
treatmenttreatment
7. Case continuedCase continued
Now I was asked by the consultant physicianNow I was asked by the consultant physician
– Are these symptoms related to kidney failure?Are these symptoms related to kidney failure?
– Can such a mild degree of renal failure (Can such a mild degree of renal failure (creatininecreatinine
of only 2.4of only 2.4) cause these symptoms?) cause these symptoms?
– What is the cause of renal dysfunction?What is the cause of renal dysfunction?
– Should we do a kidney biopsy?Should we do a kidney biopsy?
We will answer all these questions at the end of ourWe will answer all these questions at the end of our
discussion, and you can easily help me with this.discussion, and you can easily help me with this.
8. Definition of Chronic Kidney Disease (CKD)Definition of Chronic Kidney Disease (CKD)
Vs FailureVs Failure
CKD is defined as either kidney damage or
GFR < 60 ml/ min for 3 months.
Kidney Damage:
– pathological abnormalities or markers of
damage- includes blood,
– Urine: RBCs, Blood or proteins
– or imaging (eg USG showing renal
abnormalities
9. Definition: Kidney Disease outcomeDefinition: Kidney Disease outcome
Quality Initiative (K/DOQI)Quality Initiative (K/DOQI)
StageStage DescriptionDescription GFR((mL/min/1.73 m2GFR((mL/min/1.73 m2))
II Kidney damage with normal orKidney damage with normal or
increased GFRincreased GFR
9090
IIII Kidney damage with mildKidney damage with mild
decreased GFRdecreased GFR
60-8960-89
IIIIII Moderated decrease in GFRModerated decrease in GFR 30-5930-59
IVIV Severe decrease in GFRSevere decrease in GFR 15-2915-29
VV Kidney failureKidney failure < 15 or dialysis< 15 or dialysis
DRAWBACKS
10. Epidemiology: CKDEpidemiology: CKD
Worldwide public health problem: RisingWorldwide public health problem: Rising
USA: dialysis has increased from 10000 in 1973 toUSA: dialysis has increased from 10000 in 1973 to
> 506000 in 2006 (22 billion $ in 2006> 506000 in 2006 (22 billion $ in 2006))
Dialysis: No insurance covers itDialysis: No insurance covers it
Indian ScenarioIndian Scenario
– No National Registry data, reporting systemsNo National Registry data, reporting systems
– Only some some small observational studiesOnly some some small observational studies
– Prevalence of CKD:Prevalence of CKD: 0.79 to 0.87%:0.79 to 0.87%: alarming numberalarming number
– Dialysis:Dialysis: 150 to 250 per million150 to 250 per million..
11. Epidemiology: Indian ScenarioEpidemiology: Indian Scenario uhnuhn
Reasons:Reasons:
– Longer survival:L better Rx of ents with DM,Longer survival:L better Rx of ents with DM,
HT, heart disease, leading to involvement ofHT, heart disease, leading to involvement of
the kidneys in the later stagethe kidneys in the later stage
– Increased awareness: more detectionIncreased awareness: more detection
– Aging populationAging population
12. Epidemiology: Indian ScenarioEpidemiology: Indian Scenario
All CKD cases can progress to ESRD-All CKD cases can progress to ESRD-
unless identified early, and aggressive effortsunless identified early, and aggressive efforts
to slow the progressionto slow the progression
We all know the expenses… HD and TxWe all know the expenses… HD and Tx
So our best effort would beSo our best effort would be
– Prevention: Early recognition and referral toPrevention: Early recognition and referral to
nephrology services, is the keynephrology services, is the key
– Slowing the progression of CKD to ESRDSlowing the progression of CKD to ESRD
uhn
13. Risk FactorsRisk Factors
DM type 2: upto 40 % on dialysis have ESRDDM type 2: upto 40 % on dialysis have ESRD
secondary to DM 2secondary to DM 2
HT and Peripheral vascular diseases- leading toHT and Peripheral vascular diseases- leading to
atherosclerotic renal artery stenosis and ischemicatherosclerotic renal artery stenosis and ischemic
nephropathynephropathy
Obesity- hyperfiltration injuryObesity- hyperfiltration injury
SmokingSmoking
HyperlipidemiaHyperlipidemia
14. CausesCauses
Any kind of injury that causesAny kind of injury that causes
permanent damage to thepermanent damage to the
kidneys results in Chronic Renal Failurekidneys results in Chronic Renal Failure
or Chronic Kidney Diseaseor Chronic Kidney Disease
15. Adaptive hyperfiltration
(↑ PGC → maintenance of GFR)
Initial injury
(GN, ATN, AIN)
↓
Loss of renal parenchyma
↓
↓
Long-term damage
to remaining nephrons
↓
Proteinuria,
progressive renal
insufficiency
16. Main categories- Pre RenalMain categories- Pre Renal
Pre- RenalPre- Renal
– True Volume depletion:True Volume depletion: Bleeding, diarrhea,Bleeding, diarrhea,
volume depletion due to any causevolume depletion due to any cause
– Effective circulating volume depletion:Effective circulating volume depletion:
CirrhosisCirrhosis
Chronic congestive heart failure:Chronic congestive heart failure:
– Renin angiotensin aldosterone (RAAS) activationRenin angiotensin aldosterone (RAAS) activation
– leading to permanent kidney damage secondary toleading to permanent kidney damage secondary to
interstitial fibrosisinterstitial fibrosis
17. Concept of effective circulating volumeConcept of effective circulating volume
5 L container
5 L H2O
5 L container
5 L H2O
Empty part
5 L H2O
5 L H2O
18. Hypovolemia or hypotensionHypovolemia or hypotension
⇓⇓
Release ofRelease of ReninRenin from the JGA of Kidneysfrom the JGA of Kidneys
⇓⇓
AngiotensinogenAngiotensinogen release and gets converted torelease and gets converted to angiotensin1angiotensin1
in the liverin the liver
⇓⇓
Angiotensin 1 converted toAngiotensin 1 converted to angio 2angio 2 in kidneysin kidneys
⇓⇓
Angio 2 acts on glomerular blood vessels to causeAngio 2 acts on glomerular blood vessels to cause
vasoconstiction, tovasoconstiction, to maintain GFRmaintain GFR
⇓⇓
But at the same time activatesBut at the same time activates cytokines and causes fibrosiscytokines and causes fibrosis
of the Kidneys, if persistentof the Kidneys, if persistent
20. Main categories- RenalMain categories- Renal
Renal VascularRenal Vascular
– Large blood vesselsLarge blood vessels
Renal artery stenosis- atherosclerotic or other causesRenal artery stenosis- atherosclerotic or other causes
Benign NephronosclerosisBenign Nephronosclerosis
– Smaller Blood VesselsSmaller Blood Vessels
Malignant hypertensionMalignant hypertension
Vasculitis- eg Systemic lupus erythromatosis (SLE)Vasculitis- eg Systemic lupus erythromatosis (SLE)
HUS and TTPHUS and TTP
21. BL renal artery stenosis causing ischemicBL renal artery stenosis causing ischemic
nephropathy and severe Hypertensionnephropathy and severe Hypertension
32. Elevated Uric Acid Increases the Risk forElevated Uric Acid Increases the Risk for
Kidney DiseaseKidney Disease
The risk for kidney disease increased:The risk for kidney disease increased: 6 to 7 mg/dl6 to 7 mg/dl
in women andin women and 7 to 8 mg/dl7 to 8 mg/dl in menin men
Concluded that: elevated levels of uric acidConcluded that: elevated levels of uric acid
independently increase the risk for new-onset kidneyindependently increase the risk for new-onset kidney
diseasedisease
So Uric acid needs to be checked in high riskSo Uric acid needs to be checked in high risk
patients like DM and HT and treated if highpatients like DM and HT and treated if high
J Am Soc Nephrol 19: 2407–2413, 2008
33. Acute Kidney Injury Increases Risk of ESRDAcute Kidney Injury Increases Risk of ESRD
among elderlyamong elderly
Elderly individuals with AKI (ARF due toElderly individuals with AKI (ARF due to
ATN), particularly those with previouslyATN), particularly those with previously
diagnosed CKD, are at significantlydiagnosed CKD, are at significantly
increased risk for ESRDincreased risk for ESRD
suggesting that episodes of AKI maysuggesting that episodes of AKI may
accelerate progression of renal disease.accelerate progression of renal disease.
J Am Soc Nephrol 20: 223–228, 2009
34. Changes in Body Weight Predict CKDChanges in Body Weight Predict CKD
in Healthy Menin Healthy Men
increases in body weight are independentlyincreases in body weight are independently
associated with an increased risk for CKD.associated with an increased risk for CKD.
Risk remained significant even after otherRisk remained significant even after other
causes like DM, HT , metabolic syndrome etccauses like DM, HT , metabolic syndrome etc
were ruled out (adjusted)were ruled out (adjusted)
J. Am. Soc. Nephrol. 2008
35.
36. PRESENTING MANIFESTATIONSPRESENTING MANIFESTATIONS
Signs and symptoms resulting directly fromSigns and symptoms resulting directly from
alterations in kidney function:alterations in kidney function:
– decreased or no urine outputdecreased or no urine output
– flank painflank pain
– EdemaEdema
– HypertensionHypertension
– discolored urine- Hematuria, pus in urinediscolored urine- Hematuria, pus in urine
– AnemiaAnemia
37. PRESENTING MANIFESTATIONSPRESENTING MANIFESTATIONS
Symptoms and/or signs of renal failure:Symptoms and/or signs of renal failure:
– weakness & easy fatigue (anemia & uremia)weakness & easy fatigue (anemia & uremia)
– Anorexia, Nausea & vomitingAnorexia, Nausea & vomiting
– mental status changes or seizuresmental status changes or seizures
– Anasarca- fluid overloadAnasarca- fluid overload
– Bone pains & fractures after minimum traumaBone pains & fractures after minimum trauma
– Burning feet, restless leg syndrome from uremicBurning feet, restless leg syndrome from uremic
polyneuropathypolyneuropathy
38. PRESENTING MANIFESTATIONSPRESENTING MANIFESTATIONS
Symptoms and/or signs of renal failure:Symptoms and/or signs of renal failure:
– Dyspnea, orthopnea or PND: fluid accumulating inDyspnea, orthopnea or PND: fluid accumulating in
the lungs andthe lungs and Uremic CardiomyopathyUremic Cardiomyopathy
– Acidotic breathing (Rapid and deep)- due toAcidotic breathing (Rapid and deep)- due to
acidosisacidosis secondary to renal failure.secondary to renal failure.
– Chest pain/ pericardial rubChest pain/ pericardial rub: uremic pericarditis: uremic pericarditis
– Severe itchingSevere itching due to Uremia and dry skindue to Uremia and dry skin
– MalnutritionMalnutrition in advanced renal diseasein advanced renal disease
39. PRESENTING MANIFESTATIONSPRESENTING MANIFESTATIONS
Systemic symptoms due to disease causingSystemic symptoms due to disease causing
renal failure:renal failure:
– eg fever, Joint pains, skin rash in vasculitis (egeg fever, Joint pains, skin rash in vasculitis (eg
SLE, ANCA vasculitis)SLE, ANCA vasculitis)
– eg high grade fever, low BP and shock ineg high grade fever, low BP and shock in
pyelonephritispyelonephritis
42. PRESENTING MANIFESTATIONS:PRESENTING MANIFESTATIONS: Lab findingsLab findings
CBC- normocytic normochromic anemiaCBC- normocytic normochromic anemia
HyperkalemiaHyperkalemia
Urea and creatinineUrea and creatinine
Low Ca, high P and uric acidLow Ca, high P and uric acid
UrinalysisUrinalysis- Proteinuria, hematuria, pus cells, casts- Proteinuria, hematuria, pus cells, casts
Sr Albumin- Nephrotic syndromeSr Albumin- Nephrotic syndrome
Sr Cholesterol- high in Nephrotic syndromeSr Cholesterol- high in Nephrotic syndrome
44. ProteinuriaProteinuria
Normal:Normal:
– Total protein < 150 mg/dTotal protein < 150 mg/d
– Urine albumin < 10 mg/dayUrine albumin < 10 mg/day
Proteinuria =Proteinuria = > 300 mg/d> 300 mg/d
– Microalbuminuria = 30-300 mg/dMicroalbuminuria = 30-300 mg/d
– The normalThe normal Urine Protein To Creatinine RatioUrine Protein To Creatinine Ratio is lessis less
thanthan 0.2 mg/mg0.2 mg/mg. (proteins and creatinine are measured. (proteins and creatinine are measured
in mg %)in mg %)
– Micral test for Microalbuminuria detectionMicral test for Microalbuminuria detection
47. Microalbuminuria and risk of progression of
kidney disease
An early decline in GFR occurred in
– 68% with progression of MA
– 32% with stabilization of MA
– 16% with regression
– and 9% with normoalbuminuria.
J Am Soc Nephrol. 2007 Apr;18(4):1353-61. Epub 2007 Feb 28.
50. Pus cells and pus cell castPus cells and pus cell cast
Pus cells White cell casts
51. Acute Vs Chronic: Disease DurationAcute Vs Chronic: Disease Duration
The distinction between acute, rapidly progressiveThe distinction between acute, rapidly progressive
(subacute), and chronic kidney disease is arbitrary(subacute), and chronic kidney disease is arbitrary
Rise in the plasma creatinine concentration or anRise in the plasma creatinine concentration or an
abnormality on the urinalysis that has developedabnormality on the urinalysis that has developed
– within hours to days: acute processwithin hours to days: acute process
– Over days to weeks- SubacuteOver days to weeks- Subacute
– Over Months- ChronicOver Months- Chronic
Arbitory: No previous valuesArbitory: No previous values
53. RadiologyRadiology
X- Ray KUB- Renal calculus diseaseX- Ray KUB- Renal calculus disease
USG and dopplerUSG and doppler
– Size: most important feature, EchogenesitySize: most important feature, Echogenesity
– Obstruction & other structural abnormalitiesObstruction & other structural abnormalities
– Renal vessels- Renal artery and venous lesionsRenal vessels- Renal artery and venous lesions
CT scan- Replaced IVP to a large extentCT scan- Replaced IVP to a large extent
– Accurate assessment of renal stonesAccurate assessment of renal stones
– Some structural abnormalities more clearlySome structural abnormalities more clearly::
Malignancy, cysts, abscessMalignancy, cysts, abscess
54. RadiologyRadiology
MRI and MR angiographyMRI and MR angiography
– More accurate assessment of the renal arteryMore accurate assessment of the renal artery
and veins forand veins for stenosis or thrombosisstenosis or thrombosis
55. Kidney BiopsyKidney Biopsy
The most specific diagnostic test for causeThe most specific diagnostic test for cause
and prognosisand prognosis
The kidneys should be normal sized onThe kidneys should be normal sized on
USG before you biopsy itUSG before you biopsy it
Provides adequate diagnostic informationProvides adequate diagnostic information
in 90 % of the casesin 90 % of the cases
56. Complications of renal failureComplications of renal failure
Cardiac:Cardiac:
– CMPCMP
– pericarditis & tamponadepericarditis & tamponade
Nervous system:Nervous system:
– Encephalopathy, seizuresEncephalopathy, seizures
– NeuropathyNeuropathy
HematologyHematology
– Anemia of CKDAnemia of CKD
Bone and jointsBone and joints
– Renal bone diseaseRenal bone disease
– Secondary hyper PTHSecondary hyper PTH
– GoutGout
EndocrineEndocrine
– Sexual dysfunctionSexual dysfunction
– Thyroid abnormalitiesThyroid abnormalities
VascularVascular
– Vascular calcificationVascular calcification
– Severe peripheralSevere peripheral
vascular diseasevascular disease
– PrematurePremature
atherosclerosisatherosclerosis
– Severe CADSevere CAD
57. Estimating Kidney function: GFR andEstimating Kidney function: GFR and
Creatinine clearanceCreatinine clearance
Sr Creatinine:Sr Creatinine:
– insensitive markerinsensitive marker
– Needs to be corrected for age, gender, weightNeeds to be corrected for age, gender, weight
and muscle massand muscle mass
Cockcroft-Gault equationsCockcroft-Gault equations
Cret Clearance = (140-age) X weight
72 X Sr Creat
Multiply this by 0.85 in case of females
58. Measurement of GFRMeasurement of GFR
CreatinineCreatinine
eGFR (Cockcroft-Gault, MDRD)eGFR (Cockcroft-Gault, MDRD)
Creatinine ClearanceCreatinine Clearance
Creatinine Clearance + CimetidineCreatinine Clearance + Cimetidine
Radionuclide MarkersRadionuclide Markers
Inulin ClearanceInulin Clearance
Cystatin CCystatin C
59. Cockcroft-Gault equationsCockcroft-Gault equations
70/F, weight 45 kgs and 35/M, weight 70 kg70/F, weight 45 kgs and 35/M, weight 70 kg
Both have Sr Creatinine of 2 mg %Both have Sr Creatinine of 2 mg %
– In the young man, creatinine clearance / GFRIn the young man, creatinine clearance / GFR
using the formula isusing the formula is 51.36 ml /min51.36 ml /min
– In the older lady, the creatinine clearance /In the older lady, the creatinine clearance /
GFR is……..GFR is……..
18.61 ml / min18.61 ml / min
60. Back to our caseBack to our case
So can we explain all the symptoms on theSo can we explain all the symptoms on the
basis of mild renal dysfunction??basis of mild renal dysfunction??
Lets calculate the GFRLets calculate the GFR
4 months before she presented to us, creat4 months before she presented to us, creat
was1.4 mg %was1.4 mg %
– eGFR = 29.9 ml/ mineGFR = 29.9 ml/ min
Now the creat was 2.4 mg %Now the creat was 2.4 mg %
– eGFR = 17. 4 ml / mineGFR = 17. 4 ml / min
61. Back to our caseBack to our case
USG of abdomenUSG of abdomen
– RK- 7 X 2.9 cms, LK- 7.3 X 3 cmsRK- 7 X 2.9 cms, LK- 7.3 X 3 cms
– Small and echogenicSmall and echogenic
ManagementManagement
– Anemia correction & bone protection,Anemia correction & bone protection,
– control of HT and hyperlipidemia: ACEIs,control of HT and hyperlipidemia: ACEIs,
– Diet and correct acidosisDiet and correct acidosis
– AV fistula and preparation for dialysisAV fistula and preparation for dialysis
– Sister as a potential kidney donor for transplantSister as a potential kidney donor for transplant
62. ManagementManagement
Aggressive control of risk factorsAggressive control of risk factors
Smoking cessationSmoking cessation
BP target: < 125/75 in proteinuricsBP target: < 125/75 in proteinurics
Lipid target- StatinsLipid target- Statins
DietDiet modification- as per the blood chemistry,modification- as per the blood chemistry,
fluid status and symptomsfluid status and symptoms
63. ManagementManagement
CardiacCardiac evaluation and protectionevaluation and protection
– Overlapping risk factorsOverlapping risk factors
Symptomatic treatmentSymptomatic treatment
– AcidosisAcidosis
– Bone protectionBone protection
– Correction of hyperphosphatemia, low calciumCorrection of hyperphosphatemia, low calcium
– Vitamin supplementsVitamin supplements
– Anemia management: erythropoitin and IV ironAnemia management: erythropoitin and IV iron
64. Management- Proteinuria reductionManagement- Proteinuria reduction
ACEI inhibitors:
– BP control + proteinuria reduction + cardiac protection
– Ramipril: Cardiopril
ARBs
– BP control + proteinuria reduction + cardiac protection
– Telmisartan: Telsartan
High dose statins: Atocor (Atorvastatin):
– Proteinuria reduction + endothelial protection
65. Management-Renal function preservationManagement-Renal function preservation
ACEI
– Ramipril ( Cardiopril) helps slow the progression
of renal dysfunction, in addition to decrease in
proteinuria
ARBs
– Telmisartan (Telsartan): slows progression of
renal disease
– Many trial supporting the same
66. ManagementManagement
Treatment of specific diseasesTreatment of specific diseases
– Eg Steroids for SLEEg Steroids for SLE
– Specific therapy of Nephrotic syndrome: steroids,Specific therapy of Nephrotic syndrome: steroids,
cyclophosphamide, cyclosporincyclophosphamide, cyclosporin
This is the overview of my presentation. First we will discuss an interesting case, we will define the disease, risk factors and complications, how do we suspect the disease and finally management
10 yrs and 6 yrs.
Widal, PS for MP was negative. Although the LFTs were normal- she was treated with some alternative medications as jaundice.
She could not tolerate AKT and felt more nauseated, and so she stopped it on her own after 2 weeks
In the last few years, the nephrology community is prefering the term CKD instead of CRF. Because in the term CRF, the word is failure, and CKD the word is disease. And disease appears to be less bad work than failure. Failure indicates that everything has failed and nothing can be done.
This staging system was aimed at promoting early detection and treatment of CKD. This staging system applies for patients greater than 2 yrs age.
But there are many deficiencies in this defination. Eg if we have a child with nephrotic syndrome who has proteinuria for more than 3 months, but later completely responds to steroids- can he said to have CKD?
Give the example of a patient of transplant- any structural abnormalities in the kidney is said to be CKD. Eg a person born with a single kidney is functioning very well till the age of 50 yrs, he is detected to have a single kidney because an USG for done for some vague abdominal pain- Is he having CKD? Is a person who has a well performing kidney transplant having CKD- just because he has a single kidney.
SO although this defination is not very accurate, it helps staging the patient and referral practice
In the place I worked previously, ie university hospital in toronto, the size of the dialysis unit was hugh- 60 machines. And it used to run in 3 shifts. The 3rd shift was more than half empty. So I asked the director of the unit that why was the unit expanded? He told me, in 1995, when the health planners met, it was expected that the number of people on dialysis would rise and even this unit would not suffice. At the same time they started a nation wide programe for early detection and aggressive management of CKD patients. By 2000 the number of patients reaching dialysis had plateaued, and by 2007 they actually saw a decresing trend in patients requiring dialysis because of the aggressive steps they had taken to control the factors and slow progression
So when there is loss of renal parenchyma, there are less number of glomeruli, so there is adaptive hyperfiltration- because the remaining glomeruli have to take up the total load
Although the total amount of water in the container has not decreased, the size of the container has increased, so the container is relatively empty.
This happen acutely in sepsis- where there is significant capillary and venous dilatation, so the total capacity of the vascular bed is increased, although the total blood volume is the same, so here the effective circulating volume is decreased.
Similarly this happens chronically in Cirrhosis of liver and CHF. In cirrhosis- there is significant dilatation of the GI/ splanchnic blood vessels and so relative volume deficiency or effective circulating volume deficiency. Similarly in CHF, although the patient is edematous, and there is increase in the total water in the body. But the heart does not pump adequate blood, so there is less blood supply to the kidney, as if there is dehydration, again activation of the RAAS and so initially acute, and then chronic damage to the kidney.
And now we can know why we use ACEI like rami and Angiotensin 2 receptor blockers like losartan and telmisartan. They block the formation or action of angiotensin 2 and prevent the long the term damage and fibrosis.
Here the blood supply to the kidney decreases and the kidneys become ischemic, causing direct damage to the kidneys. Also there is activation of renin- angiotensin and aldosterone system, causing fibrosis of the renal tissue
Malig HT causes severe vascular damage and the blood vessels close down and the glomeruli become ischemic and sometime necrotic leading to renal failure
It is very important to identify the last cateogary, as they are very much treatable if identified within the first week to 10 days, and reach a stage of permanent dialysis with in 1 month if not treated aggressively.
This is a more advanced stage of diabetic nephropathy, where whole of the glomerular structure is replaced by pink hyaline matrix- because of Diabetes
This is what we call RPGN in Nephrology and this is an Nephrological emergency- because if not treated within a few days, these patients reach end stage renal disease. They present as HT, edema, anemia, normal sized kidneys on USG, proteinuria+ RBCs + RBC casts in urine and rapidly become oligouric. They need dialysis, high dose steroids, cyclophosphamide and plasma exchange. And are very much treatable
We underestimate renal calculus disease as the cause of renal failure. Even though there is ureteric obstruction causing obstructive nephropathy and renal failure, and recover after relief of obstruction, each episode leaves some residual damage, especially due to infection.
Also non obstructive Renal calculus present in the kidneys induce fibrosis and cause chronic renal failure-
Heavy interstitial infiltrates with normal glomerulus- this is mainly caused by drugs like NSAIDS (diclomol or brufen) and antibiotics- especially penicillins and cephalosporin&apos;s, which are commonly used. This condition is diagnosed by History, urine analysis, and kidney biopsy
A plain CT scan of the abdomen is a very good investiagations for those presenting with colic, many a times this can be missed on a routine abdomen X ray.
For eg, a diabetic with creat of 1.5 mg % develops severe UTI and sepsis with ATN- is unlikely to recover completely from ARF, as compared to a younger individual
The only reason I am showing you this picture is any vasculitic rash associated with any renal abnormality can indicate a potential Crescentic GN or Rapidly progressive GN- which needs urgent identification and aggressive management
Frankly, a good and accurate urine analysis gives a lot of clues to the diagnosis. And a well performed normal urine analysis practically rules out renal disease in most cases. But the problem is not all pathologist have the time to look at the urine themselves, and a technician has never been taught how to identify casts. So I look at the urine myself under a microscope, and we have been doing this for years. It sometimes completely changes our initial diagnosis.
Lets discuss something about proteinuria.
Using a spot sample, we can avoid 24 hours urinary collection for protein estimation
It has been shown to correlate fairly well with 24 hours protein estimation.
So it looks like microalbuminuria is definitely bad
This distinction is said to be arbitory because most of the times we do not have previous values, and we find a patient with a high creatine or abnormal urine analysis for the first time.
Say there Is a person whose creatinine was 1 mg % last month and is now 3 mg %, definitely acute. But if it was 2.4 mg % 4 months ago and now 3 mg %, then it is more likely to be chronic which is slowly progressing
USG is the most utilized and most useful test for the kidneys and the Urinary bladder- its simple, readily available and non invasive. But the biggest deficiency is it totally depends on the skill of the radiologist- its very subjective
I have recently come across a lady who presently to the orthopedician with a Fracture of hip, she only had slipped and twisted her ankle. The trauma was not atall significant: she was 46 yrs old. Surgery was planned, but Hb was 7.5 g%, so a physician was consulted who asked for routine investigations. The creatinine was found to be 6.5 mg% and the kidneys were small size, indicating Chronic kidney disease. So fracture was her presenting symptom.
Sr Creatinine: this is a relatively insensitive marker. Sr Creatinine starts rising only after a significant amount of kidney function is lost. This is because : in the early stages of renal dysfunction, rise in Sr creatinine does not occur- as this is actively secreted by the kidneys, and this secretion increases in early stages and does not allow the creatinine to rise. This does not mean that the renal function is normal. Also this needs to be corrected for age, gender and weight and muscle mass. There is a difference in GFR between 2 people with the same creatinine. So we have deviced various formulas
There are a number of available ways to estimate the GFR including
the serum Creatinine
Creatinine Clearance
Creatinine Clearance + Cimetidine
Inulin Clearance
Radionuclide Markers
Cystatin C
Now lets calculate the creatinine clearance in the older lady.
There have been many more complex formulas for calculating eGFR, most of them have been used for adjusting doses of medications
So we could very well explain the symptoms on the basis of a creatinine of 2.4 mg % and what was referred to us as mild renal dysfunction
Many a times, the dietician presecirbes a general “ Renal diet to the patient”, but most of the patients are not eating well, and there protein intake is much less than the recommanded. In the western world, the protein intake might be in the range of 2 gm/ kg. in our normal diet its less than 1gm/ kg. already the patient is eating less, and we restrict them further on many things and they get malnutrited.
So each patient requires and individualized dietary prescription, depending on what is eating at present.
You may ask this question- on one hand I am saying that ACEI and ARBs are good for the kidneys. Yes they are because they inhibit the RAAS – which is responsible for fibrosis of the kindeys, endothelial damage and cardiac failure. But in those who have critically low GFRs, the GFR is angio 2 dependent. So inhibiting it will cause acute worsening of the GFR. We accept upto 25 % increase in GFR after starting ACEI and ARBs and closely monitor the renal function and electrolytes
CAD and sudden cardiac death is the leading cause of death in CKD patients, so monitoring for cardiac risk factors is very important.
Hyperphosphatemia is associated with calcification of the blood vessels. The blood vessels become like hard pipes made of calcium, and is seen prominantly on X- rays of the hand, abdomen