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DIABETIC NEPHROPATHY Izharul Hasan Presenter Faiyaz Ahmed*  Co-presenter M.Zulkifle HOD & Reader Haseeb A. Ansari Lecturer Dept. Of Tahaffuzi wa Samaji Tib, National Institute of Unani Medicine Bangalore * Govt. Nizamia Tibbi college, Hyderabad [email_address] +919379559363 International Conference of Integrative Medicine & 1 st   SAARC Conference on Unani Medicine  Introduction ,[object Object],[object Object],abolic  control may  not  develop  clinical  diabetic  nephropathy 4 Context:  Each  kidney  is  made  of  hundreds  of  thousands  of  filtering  units  called nephrons.  Each  nephron  has  a  cluster  of  tiny  blood  vessels  called  a glomerulus.  Together  these  structures  help  remove  waste  from  the  body.  Too much  blood  sugar  can  damage  these  structures,  causing  them  to  thicken  and become  scarred.  Slowly,  over  time,  more  and  more  blood  vessels  are destroyed.  The  kidney  structures  begin  to  leak  and  protein  (albumin)  begins  to  pass  into  the  urine.  Clinically,  DN  is  characterized  by  a  progressive increase  in  proteinuria  and  decline  in  GFR,  hypertension,  and  a  high  risk  of cardiovascular  morbidity  and  mortality. The  earliest  clinical  evidence  of  nephropathy  is  the  appearance  of  low  but abnormal  levels  (>30 mg/day)  of  albumin  in  the  urine,  referred  to  as microalbuminuria,  and  patients  with  microalbuminuria  are  referred  to  as  having incipient  nephropathy.  Diabetic nephropathy  is  a  leading  cause  of  end  stage renal  failure.  The  pathogenesis  of  diabetic  nephropathy  is  multifactorial  with contribution  from  metabolic  abnormalities,  homodynamic  alteration,  and  various growth  factors  and  genetic  factors.  Epidemiologic  and  family  studies  have demonstrated  that  family  clustering  and  ethnicity  plays  an  important  role  in  the  risk  of  developing  this  kidney  disease. 1   It  is  estimated  that  up  to  50% patients  with  diabetes  mellitus  will  develop  renal  failure 2 .  It  is  now  firmly established  that  diabetic  nephropathy  is  associated  with  high  morbidity  and  mortality 3.   There  is  marked  heterogeneity  in  the  clinical  picture  seen  in  long termed  diabetes  as  some  diabetic  patients  even  with  poor  metabolic  control may  not  develop  clinical  diabetic  nephropathy 4 Risk  factors  for  development  and  progression  of  diabetic  nephropathy Before  the  widespread  aggressive  treatment  of  blood  pressure    and  hyperglycemia,  between  25% and  40%  of  both  type 1  and  type   2  patients  developed  diabetic  nephropathy  over  the  course  of    25  years 5,6,7  and  risk  factors  that  differentiate  this  subgroup    from  patients  who  maintain  normal  renal  function  are  systemic    hypertension,  glycaemic  control, gender  (M>F), genetic factors, hyperlipidaemia, dietary protein intake and smoking. Blood pressure:  Hypertension  is  strongly  associated  with  insulin  resistance,    even  in  the  absence  of  diabetes,  and  some  40-70%  of  type 2  patients    will  become  hypertensive  during  their  disease. Glycaemic control:  Type 1  and  type 2  diabetes  have  in  common  the  state  of  chronic  hyperglycaemia,    and  glucose- dependent  processes  are  likely  to  be  involved  in  the    pathogenesis  of  diabetic  complications,  including  nephropathy.  Glucose- induced    tissue  injury  may  be  mediated  by  the  generation  of  advanced  glycated    proteins  or  via  other  mechanisms  such  as  the  polyol  pathway,    both  of  which  have  been  implicated  in  nephropathy. Proteinuria:  Proteinuria  is  generally  regarded  as  a  marker  for  the  degree    of  glomerular  damage:  the  level  of proteinuria  correlates  well    with  the  prognosis  for  renal  function,  and  interventions  that    retard  the  progression  of  diabetic  renal  disease  also  reduce    proteinuria.  However,  we  do  not  yet  know  whether  the  flux  of    protein  across  the  glomerular  basement  membrane  is  causally    implicated  in  the  evolution  of  diabetic  renal  disease  or  simply    reflects  glomerular  damage. Genetic Factors:  Genetic  factors  are  likely  to  be  important  in  diabetic  nephropathy.    Recent  interest  has  focused  on  genes  of  the  renin  angiotensin    system,  which  are  known  to  be  highly  polymorphic  and  have  been    extensively  studied  in  relation  to  cardiovascular  disease.  Hyperlipidemia:  Hyperlipidaemia  is  common  in  both  type 1  and  type 2  diabetes.    Raised  plasma  triglycerides  and  low  levels  of  highdensity  liproproteins   (HDL)  have  been  correlated  with  the  development  of  diabetic    nephropathy  as  well  as  with  cardiovascular  diabetic  complication. Material and methods : 35  patients  of  type  2DM  with  clinical  Nephropathy  were  taken  at  TDF (TRIAL DRUG  FORMULA)  for  120  days  &  creatinine  clearance  test  was repeated  for  every  30 days.  TDF,  especially  prepared  with  the  aim  to  modulate  impaired  kidney  function  contains  musaffi,  muhallil,  mufattah  and  mudir  advia.  A  total  of  54  patients  were  interviewed  for  data  collection,  of  which,  31  were males  and  23  were  females.  Specific  questionnaire  was  used  which  included variety  of  questions,  such  as  present  age  of  the  patient,  age  at  diagnosis  of  nephropathy,  age  at  diagnosis  of  diabetes,  total  duration  of  diabetes,  familial  relationship  between  husband  and  wife,  familial  relationship  between  the  parents  of  patients,  family  history  regarding  the  same  or  any  other  disease,  information  regarding  different  clinical  tests  done  for  the  diagnosis  of  nephropathy  and  information  about  the  socio  economic  status  (occupation),  education  and  life  style  of  the  patients. Height  and  weight  of  the  patients  were  studied  in  order  to  check  their  link  with  the  prevalence  of  disease.  Height  was  measured  in  meters  while  weight  was  recorded  in  kg.  Clinical  tests  included  blood  urea,  serum  creatinine,  blood  glucose,  sodium,  potassium,  and  albumin.  Statistical  analysis  like  mean, standard  error,  number  of  studied  samples (n),  t-test  and  percentage (%)  were  also  carried  out  during  our  study.  For  control  studies  regarding  diabetes  and  diabetic  nephropathy,  20  normal  subjects  were  interviewed  to  have  a  complete  comparative  analysis. Results:  After  120  days In  65.71 %  patients  with  mild  and  moderate  renal  impairment  normal creatinine  clearance  was  obtained..In  patients  with  severe  renal  impairment  slow  apparent response  was seen.. Trial drug formula Dar Hald  (Berberis  vulgaris),  Mako  (Solanum nigrum),  Vaj turki (Acorus  calamus), Majeth  ( Rubia  cordifolia),  Panchang  (Chena  podium  album),  Zaravand  (Arista lochia),  Gokhru (Tribulus  terr),  Pakhan  Baid  (Saxitraga  lingulata),  Chandan  (Satalum  Album)  in  equal  amount  and  given  in  powder  form  at  a  dose  of  3 gm  two  times  daily  with  decoction  of Tukhm  Khayareen,  Tukhm  Gazr,  Tukhm  Karfas,  Chiraita,  Sarphoka,  Jadwar,  Jaifal,  Behman  surkh,  Fil  fil  siyah,  Mako, Kasini each  3gm. Conclusion  ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],A cknowledgement Dr. A.M.K Sherwani, Lecturer Dept of TST, NIUM Bangalore  Dr. Zarnigar, Lecturer dept of TST, NIUM Bangalore  Dr Malik Itrat, PG Scholar Dept of TST, NIUM bBangalore  Dr Mohd Shakir, PG Scholar, Dept of TST, NIUM Bangalore Affiliation  Dr.N.T.R.University Of Health Sciences A.P. Vijayawada, Andhra Pradesh

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