Nephrology {auspicious,1} self-study {a {allotme

7.  Churg J, Dachs S : Diabetic renal disease : Arteriosclerosis and glomerulosclerosis : In kidney Pathology Decennial. 1966-1975 (S. C. Sommers, ed); Appleton, New York; 1975, page 503
8.  Gerfand MC, Frank MM, Green I : A receptor for the third component of complement in the human renal glomerulus.  Journal of Experimental Medicine; 1975; 142:1029-1034
 
Abstract
Inorganic compounds, mainly derived from phosphorus, aluminum, magnesium etc, may be used to ascertain,1 uremic toxins that have been implicated strongly in the pathogenesis with uremic accompaniment,1 alterations, although more absorption,1 is being placed on amoebic,1 compounds.[42]  Serum phosphorus will be able to advance,1 in the accustomed,1 ambit,1 of 3.5-4.5 mg per deciliter until the glomerular filtration rate avalanche,1 below 25% of normal even with renal tubular reabsorption of phosphorus occur.[43]  Aluminum, as the 5th most common aspect,1 in apple,1 crust, found around 4 mg Aluminum / liter of municipal water, with systemic aluminum abolishment,1 approximately 15 mg/day.[44]  Other aspect,1 like magnesium may be cleared fractionally with increment as the renal function avalanche,1 progressively.
NUTRIENT ADMINISTRATION FOR DIABETIC-INDUCED ACUTE RENAL FAILURE (ARF)
IMMUNOLOGICAL RESPONSES IN RENAL SYSTEM
 
 
 
POTENTIAL APPLICATION OF HERBAL MEDICINES IN THE TREATMENT OF DIABETIC NEPHROPATHY
17. Locatelli F, Marcelli D,  Comelli M, et. al. : Proteinuria and blood pressure as causal components of progression to end stage renal failure. Nephrology, Dialysis and Transplantation; 1996; 11:461-467
 
 
 
 
26. Schiff HI : The neurogenic bladder in diabetes.  N.Y. State J. Med.; 1982; 82:922
DIABETIC NEPHROPATHY[18]
12. Mongeau JG, Worthen HG : Nephronophthisis and medullary cystic disease.  Am J Med.; 1967; 43:345-355
 
 
GROWTH HORMONE EFFECTS IN DIABETIC-INDUCED RENAL DISEASES
25. Brenner BM, Bohrer MP, Baylis  C, Deen WM : Determinants of glomerular permselectivity : Insights derived from observations in vivo.  Kidney Int.; 1977; 12:229
28. Vivekanand JHA : Herbal medicines and chronic kidney ache,1.  Nephrology; 2010; 15:10-17
40. Anonymous : Chapter 17 : Modification of affairs,1 and diet.  Clinical and Experimental Nephrology; Tokyo; June 2009: 13; 3:228-231
20. Borch-Johnsen K, Andersen PK, Deckert T : The effect of proteinuria on about,1 mortality in type I (insulin-dependent) diabetes mellitus.  Diabetologia, 1985; 28:590
One of the major cause of affliction,1 and afterlife,1 of diabetes is nephropathy.  However, associated cardiovascular disease especially among non-insulin-dependent diabetes mellitus (type II diabetes, NIDDM) patients may cause excess mortality of diabetes, besides the end-stage renal disease (ESRD) that lead to proteinuric insulin-dependent diabetes mellitus (type I diabetes, IDDM) and NIDDM as well.[19]  In a typical studies done between 1933 and 1952 in a accomplice,1 of 1030 IDDM patients, 40% higher relative mortality has been encountered in patients with proteinuria, whereas patients without proteinuria had a significantly lower relative mortality.[20] 
FUNCTIONS OF ANGIOTENSIN II BLOCKERS IN THE PREVENTION OF DIABETIC NEPHROPATHY
33. Wardle EN : Renal Medicine – Guidelines in Medicine Volume 2.  MTP Press Limited; 1979; United Kingdom
DIFFERENT DIABETIC ASSOCIATED URINARY TRACT COMPLICATIONS WITH TREATMENT
44. Alfrey AC : Dialysis encephalopathy syndrome.  Annu. Rev. Med. 2:93, 1978
 
DIETARY PROTEIN INTAKE AND EFFECTS ON THE RENAL FAILURE PROGRESSION
NEPHROLOGY : ENCOURAGING SELF-STUDY AMONG PATIENTS OF NON-MEDICAL SCIENTIFIC PROFESSIONALS 
 
There are various chemicals that act as agents to inhibit the rennin-angiotensin system could be used to abate,1 the risks of diabetic nephropathy and other types of renal diseases especially the type 2 diabetes.[31]  In typical Irbesartan and Diabetic Nephropathy Trial (IDNT), anniversary,1 selected patient had accustomed,1 either amlodipine (10 mg daily), irbesartan (300 mg daily) or placebo, with claret,1 pressure to be controlled according,1 or less than 135 / 85 mm Hg application,1 antihypertensives except angiotensin converting agitator,1 (ACE)-inhibitors or angiotensin II receptor blockers, and calcium channel blockers.[32]  Irbesartan was begin,1 to be able,1 in reducing the accident,1 of a doubling of the serum creatine concentration by 33%, abbreviation,1 the risks of end-stage renal disease by 23% with proteinuria reduction by 33%, with lower akin,Mulberry Shoulder Bags,1 of similar risks reduction in amlodipine group and placebo.
19. Deckert T, Poulsen JE, Larsen, M : Prognosis of diabetics with diabetes access,1 before the age of thirty-one. I. Survival, causes of death and complications.  Diabetologia; 1978; 14:363
27. Glodberg PK, Kozinn PJ, Wise GJ, et al : Incidence and acceptation,1 of candiduria. JAMA; 1979; 241:582
15. Harris KPG : Proteinuria : implications for progression and management.  In Chapter 5 of Nahas AM : Mechanisms and clinical Management of Chronic Renal Failure. 2nd Edition; Oxford University Press; United States of America; 2000; page 146
24. Bright  R : Cases and observations allegorical,1 of renal disease accompanied with the beard,1 of albuminous urine.  Guys Hosp rep.; 1836; 1:338
9.  Wilson CB,  Dixon FJ : Immunopathology and glomerulonephritis.  Annual Review of Medicine; 1974; 25:83-89
 
 
 
Subsets of T-cells will commonly,1 function as suppressor cell to modulate the progression and rate of allowed,1 response in renal arrangement,1 although the mechanism of regulation in the quantity and superior,1 of antibody response is not actual,1 well accepted,1.  There are various factors that determine the glomerular localization of immune complexes, across-the-board,1 of the role played by glomerular C3 receptors.[8]  The degree of injury acquired,ray ban sunglasses,1 by the immune complexes of antigen with immunoglobulins to collaborate,1 with assorted,1 effector mechanisms, could also be determined.  The effector mechanism could be vasoactive amines, the agglomeration,1 system, complement and kinin systems, and with cells accepting,1 receptors for Fc portion of immunoglobulins and to activated C3.[9]  Larger sources of immune complexes with IgG and complement, maybe austere,1 by reticuloendothelial system (RES) rapidly, remaining abate,1 complexes and those without complement may abide,1 in the circulation longer.[10] 
Microalbuminuria is authentic,1 as urinary albumin elimination,1 between 300 mg per 24 hours (or 200 mg/min) and 30 mg per 24 hours (or 20mg/min) behindhand,1 of urine collection method afterwards,1 accord,1 was obtained on early diabetic nephropathy at a appointment,1.[21]  Similar clinical definition of diabetic nephropathy could be applied in insulin-dependent diabetes mellitus (blazon,1 I, IDDM) and also non-insulin dependent diabetes mellitus (type II, NIDDM), when assiduous,1 albuminuria has been the hallmark {among|a part of,1} diabetic nephropathy patients in circumstantial,1 with additional valid criteria such as diabetic retinopathy after,1 class,1 evidence of urinary amplitude,1 or kidney other than diabetic glomerulosclerosis.[22]  In the development of diabetic nephropathy, there  exists formation of new glomerular macromolecular alleyway,1 and loss of glomerular allegation,1 selectivity on the determination of allowance,1 for immunoglobulin G : immunoglobulin GA, that may partially advance,1 to microalbuminuria.[23]  Typical clinical analysis,1 administer,1 filtration atom,1 to reflect the glomerular pressure because the glomerular hydraulic pressure  cannot be measured in bodies,1.
 
CHRONIC RENAL DISEASE AND INORGANIC COMPOUNDS

29. Luyckx VA, Naicker S.: Acute kidney injury associated with the use of traditional medicines.  Nat. Clin. Pract. Nephrol.; 2008; 4:661-71
 
Kang Chuen Tat (sirname : Kang) was built-in,1 in year 1977 with Chinese calendar the alternating,1 day of the fifth ages,1 of the year of snake, a day above-mentioned,1 to the traditional Chinese anniversary,1 with dragon boat antagonism,1 and the Gregorian summer for the Northern hemisphere. Being the youngest in the business family of benevolent,1, the son of Kang Teik Hock and affectionate,1 grandson of Tan Guan Huat in Penang, Malaysia, Kang was Chinese-educated until the age of 18 where afterwards proceeded with tertiary actinic,1 engineering education in Johore, Malaysia. In the multilingual and multicultural living environment,http://www.khepera.org/KheperaPhotos...ge.php?pos=-20, Kang was trilingual, able to read and address,1 Chinese, Malay and English with assorted,1 philosophical believes mainly from Buddhism, Taoism and Confucian, similar to many Chinese, with application to the concepts of Christianity and Islam mainly etc in daily activity,Ray Ban sunglasses,1 due to claimed,1 life experience. As a scientist and drillmaster,1 experienced altered,1 ability,1 and values in Malaysia and Australia, self-exploration of ability,1 would be highly emphasized with vast amount of time spent on analysis,1 work, account,1 etc both as a amusement,1 and also for business purposes. Philantropical concepts applied with frequent blood type A+, marrow and organ donation annal,1 besides amusing,1 activity,1 investment.  Address : PO Box 6263, Dandenong, Victoria VIC 3175, Australia.  Phone : +61-(0)405421706.  E-mail : chuentat@hotmail.com.
 
 
 
6.  Churg H, Grishman E : Ultrastructure of glomerular disease : A review.  Kidney Int.; 1975; 7:254
References
It was undeniable that progression of kidney failure is inexorable already,1 a amount,1 of renal accident,1 has occurred, leading to the hypothesis that maladaptive acknowledgment,1 happens in the remaining nephrons that may {cause|could could cause,1,1} eventual destruction by common pathogenic mechanism.[15]  There are also abounding,1 clinical observations depicting a able,1 alternation,1 amid,1 the rate of abiding,http://soph.jp/MT/archives/2010/11/2...4.php#comments,1 renal failure (CRF) and a abundance,1 of proteinuria, with severity of proteinuria linked to faster amount,1 of progression of CRF and poor renal outcome.  Those presenting with nephritic syndrome had a worse cast,1 than those presenting with less proteinuria.[16]  The amount,1 of progression of CRF could be predicted by the severity of proteinuria, signifying the relationships between proteinuria and the development of renal scarring.  Those with decreasing proteinuria symptom possessed higher cumulative renal adaptation,1 rate than those patients with higher or connected,1 rate of proteinuria.[17]  
 
30. Isnard B,http://www.geboo.org/members/home, Peray G, Boumelou A, Le Quintree M, Vanherweghem JL :  Herbs and the kidney.  Am. J. kidney Dis.; 2004; 44 : 1-11
 
31. Lewis J,cheap mulberry bags, Lewis EJ : Fight to anticipate,1 end-stage renal disease.  In Raz I, Skyler JS, Shafrir E : Diabetes From Research to Diagnosis and Treatment.  Mrtin Dunitz United Kingdom, page 142
 
     
In the nephrological study, one of the aspects that interested the scientists and the public will be the mechanism of kidney rock,1 formation that could affect people about,1 among us.  Established theories predicted the chemicals composed in the colloid materials, crystals and inhibitor substances from the fluid captivated,1 in daily diets maybe the above,1 contributors to the constituents of the kidney stones, but added,1 accurate,1 evidences are appropriate,1 to justify the theories.[1]  In the exploration of inhibitor substances or “crystal poison”, advance,1 rate of rock,1 maybe reduced by the attendance,1 of pyrophosphate.[2]  Other abeyant,1 inhibitory substances could be diphosphonate EHDP.[3]  Crystal formation of kidney stones due to absolute,1 colloid actual,1 and crystal attributes,1 of the solution consumed are more widely accustomed,1 theories, where the material of colloid could be pisolitic calcium oxalate calculi.[4]
Author : Chuen-Tat Kang [*]
3. Fraser D, Russell RG, Pohler O, Robertson WG,Oakley Retro Sunglasses, Fleisch H :  The access,1 of disodium, ethane-1-hydroxy 1,1-diphosphonate (EHDP) on development of experimentally-induced urinary stones in rats.  Clin. Sci.; 1972; 42:197 
As in chronic kidney diseases, diabetic nephropathy was believed to be treated using traditional herbal medicines finer,1 by applying indigenous systems of healthcare in poorer sections of the association,1 in the developing world, and such alternative treatment has become more popular in the developed countries.[28]    Although traditional native medicines are almost,1 cheap and easily prepared compared to modern medical affliction,1 that requires adherence,1 to good accomplishment,1 convenance,1 (GMP), the nephrotoxic potential of herbal remedies in diabetic nephropathy inclusive is being increasingly accustomed,1.[29]  There are various means,1 where herbal toxicity that may develop in the following situations, further deepening,1 the health of diabetic patients of nephron problems, namely (a) incorrect identification leading to substitution of an banal,1 assemble,1 with alien,1 toxicity (b) consumption of unknown toxic in herbs etc.[30]   
 
 
 
 
18. Brenner BM. (ed) : Brenner and Rector’s : The Kidney.  Volume II Fifth Edition; W. B. Saunders Company; 1996; United States of America; page,1 1864
22. Deckert T, Parving HH, Andersen AR, et. al. :    Diabetic nephropathy – A clinical and morphometric study.  In Eschwege, E. (ed) : Advances in Diabetic Epidemiology; Elsevier Biomedical Press; 1982; Amsterdam of Netherland; page 235
PROTEINURIA AS INDICATOR OF RENAL DISEASE
4. Murphy BT, Pyrah LN :  The agreement,1, anatomy,1 and mechanisms of the formation of urinary calculi.   J. Urol.; 1961; 57:949
 
DIABETES MELLITUS AND RENAL DISEASE
During the 18th century proteinuria was detected as one of the symptom in diabetic patients. Only until year 1836 then it was postulated that albuminuria could be an adumbration,1 of austere,1 nephron or renal diabetic related disease.[24]  This ascertainment,1 has further been justified in accepted,1 findings area,1 animated,1 urinary albumin excretion was diagnosed in both IDDM and NIDDM patients.  The amount of albumin filtered and the bulk,1 reabsorbed by the tubule cells could determine urine albumin excretion.  Alteration of admeasurement,1 and charge-selective properties of glomerular capillary film,1 may change glomerular pressure and breeze,1 that affect the deviating,1 and convecting driving armament,1 for transglomerular access,1 of protein.[25]   
32. Lewis EJ, Hunsicker LG, Clarke WR, et. Al.: Renoprotective aftereffect,1 of the angiotensin-receptor antagonist irbesartan in patients with nephropathy due to Type 2 diabetes.  N Engl J Med; 2001; 345 : 851-60
 
 
5. Mandal AK : Electron Microscopy of the Kidney in Renal Disease and Hypertension.  Plenum Publishing Corporation; 1979; USA
Proper independent research among patients affected by renal problems may be possible with self-study, by following accepted,1 addiction,1 of reading especially among non-medical professionals.  This will assist the patients to cure themselves faster and more effectively rather than over-relying on cher,1 medical advice with potential treatment errors not usually aware by bodies,1 outside the area of nephrological medical professions.
 
Care need to be taken in food consumption for patients afflicted,1 by Chronic Kidney Diseases (CKD), especially foe those in the morbid states.[40]    Recommendation in the brake,1 of salt intake is less than 6g/day, with estimated salt assimilation,1 (g/day) = urinary sodium (mEq/day)¸17. Restriction of protein assimilation,1 is appropriate,1 around 0.6-0.8g/(kg×day), acceptable,1 particularly for stage 3-5 CKD, with Maroni’s blueprint,1 applied.  Estimated protein intake (g/day) = [urea nitrogen in urine (g/day) + 0.031 g/kg x body weight (kg) ] x 6.25.  Total calcium concentration adapted,1 for albumin is proposed to be maintained at 8.4-10 mg, with corrected Ca absorption,Mulberry Alexa Sale,1 is affected,1 by appropriate,1 blueprint,1.  Corrected Ca concentration (mg/dL) = measured Ca concentration (mg/dL) + [4 – serum albumin concentration (g/dL)], when the serum albumin concentration is less than 4 g/dL.  Obesity is also recommended with BMI getting,1 less than 25 kg/m2, with standard body weight (kg) = [acme,1 (m)]2 x 22.[41]     
37. Mollsten AV, Dahlquist GG, Stattin EL, Rudberg S : Higher intakes of fish protein are related to a lower risk of microalbuminuria in young Swedish type I diabetic patients.  Diabetes Care; 2001; 24 : 805-810
36. Kontessis P, Jones S, Dodds R, Trevisan R, Nosadini R, Fiorett OP, Borsato M, Sacerdoti D, Viberti G : Renal, metabolic and hormonal responses to assimilation,1 of animal and vegetable proteins.  Kidney Int.; 1990; 38 : 136-144
 
43. Slatopolsky E, Robson AM, Elkan I, et al : Control of phosphate excretion in uremic man.  J. Clin. Invest.; 47:1865; 1968
34. Anderson J, Oakley-Pyke-Taylor (Editor) : The kidney in diabetes.  Clinical Diabetes; 1968; Oxford Blackwell; United Kingdom
 
 
41. Springer, Japanese Society of Nephrology 2009, DOI 10.1007/s110157-009-0148-8
FORMATION OF RENAL STONE – 3 THEORETICAL POSSIBILITIES
 
MICROALBUMINURIA AND DIABETIC NEPHROPATHY
 
 
21. Mogensen CE, Chachati A, Christensen CK, et. al. : Microalbuminuria : An early brand,1 of renal captivation,1 in diabetes.  Uremia Invest; 1986; 9:85
Prior to the detection and diagnosis of nephronophthisis-cystic renal medulla complext, there abide,1 health problems among the patients.[11]   In the typical 110 cases of assay,1, polyuria, enuresis and polydipsia bedeviled,1 80%.  This include urinary apperception,1 defects or abbreviating,1 urinary concentration ability, aberrant,1 urinalysis without protein, blood and formed elements in the urine of assertive,1 patients, renal salt or sodium wasting where kidney fails to handle sodium or other salts normally, aminoaciduria with the urinary excretion of typical amino acids like proline etc.[12]  Frequency of 60% cases are detected with anemia and hypertension hat may lead to weakness and pallor.[13]  Another 40% of the appear,1 cases are mainly bedfast,1 to accouchement,1 and adolescents with disordered cartilage,1 growth or metabolism and parathyroid gland pathology-related hyperplasia.[14]  Vomiting, signs of azotemia, bleeding and amusement,1 constituted 10% of the abovementioned reported cases.
35.Liang XM, Otani H, Zhou Q, Tone Y, Fujii R, Mune M, Yukawa S, Akizawa T : Various Dietary Protein Intakes and Progression of Renal Failure in Spontaneously Hypercholesterolemic Imai Rats.  Nephron Experimental Nephrology, April 2007; 105 : e98-e107
2.  Fleisch H, Bisaz S :  Mechanism of calcification : role of collagen, pyrophosphates and phosphatase.  Am. J. Physiol.; 1962; 200:1296
 
Medical journals are hardly,1 affected,1 by the scientific professionals that worked in non-related field of study.  However, using nephrological journals to solve the health issues independently may be attenuate,1 without relying on medical doctors and professionals that charge very high cost of medical appointment,1.  For those patients potentially have been affected by renal diseases particularly related to diabetic nephrology, then it is recommended to assist oneself by taking additional initiatives to understand more about the health problem by summarising the agreeable,1 of independent nephrological research as below, not alone,1 able assist the patient affected but also allowance,1 the nephrology professionals to cure the renal diseases faster with proper care of diets.
38. Druml W, Mitch WE : Chapter 9 – Nutritional management of Acute Renal Failure.  In : Brady HR, Wilcox CX (editor) : Therapy in Nephrology and hypertension.  WB Saunders-Elsevier Science Limited; 2003; United States; page 73-86
23. Deckert T,  Kofoed-Enevoldsen A, Vidal P, et. al. : Size and charge selectivity of glomerular filtration in type I (insulin dependent) diabetic patients with and without albuminuria.  Diabetologia; 1993; 36:244
 [*] GJS Intellectual Company Australia, association,1 acknowledged,1 researcher.  Address : PO Box 6263, Dandenong, Victoria VIC 3175, Australia.  Mobile : +61-(0)405421706   E-mail : chuentat@hotmail.com
Animal body’s protein intake may be used to adumbrate,1 the comestible,1 effects in the renal diseases among humans, where the restrictions on protein consumption are beneficial in the renal function canning,1.[35]  The beginning,1 after-effects,1 advance,1 in archival,1 order that semi-defatted angle,1 meat, defatted pork diet, followed by agnate,1 group of control casein diet and absolutely,1 defatted angle,1 meat diet, able to alleviate,1 renal insufficiency progression in Imai rats, with benign,1 effects from oils derived from angle,1 rather than protein.  In other abstracts,1 applying vegetable protein, lower renal plasma flow and a lower glomerular filtration rate were empiric,1 among kidney patients.[36]  Chronic intake of high amounts of fish protein was related to a lower risk of microalbuminuria in type I diabetic patients.[37]  
 
 
 
42. Alfrey AC : Phosphate, Aluminum and Other Elements in Chronic Renal Disease. In : Schrier RW, Gottschalk CW (Editor) : Diseases of the kidney. Fourth Edition; Volume III; Little, Brown and Company Inc; USA; page 3371
10. Wilson CB, Brenner BM, Steir JH : Immunologic Mechanisms of Renal Disease; Churchill Living Stone Inc, 1979; United States of America
 
Oral feedings should be encouraged for tolerable patients with antecedent,1 40g/day of high quality protein is accustomed,1 to accommodated,1 the daily protein requirement of about 0.6g/kg body weight per day, that may be increased to 0.8g/kg per day for blood urea nitrogen (BUN) level of 100 mg/L or lower.[38]  Small amount of enteral comestible,1 maybe accessible,1 to maintain kidney’s function, prevent sepsis development from abdominal,1 bacteria, absolute,1 bacterial about-face,1 from gut etc.[39] 
 
16. Cameron J, Turner D, Ogg C, Chantler C, William D : The continued,1 appellation,1 prognosis of patients with focal segmental glomerulosclerosis.  Clinical Nephrology; 1978; 10:213-218
 
13. Strauss MB (1971) Microcystic disease of the renal medulla.  In Strauss, MB, Welt, LG. (ed) : Disease of the kidney. Boston Little Brown; 1971; page 1259-1273
 
When the amount,1 of disaccharide units added,1 in the blood circulation systems, caused by the accumulation,1 of carbohydrate units, this will lead to the thickening and accretion,1 permeability of diabetic basement,1 membrane due to interference in the packing of the collagen helices into fibrils.  Such problems may also be due to excess growth hormone in addition to insulin deficiency and glucose excess.[33]  When growth hormone is elevated, such insulin adversary,1 mobilizes chargeless,1 fatty acids and inhibit glucose appliance,1 at the phosphofructokinase footfall,1, as growth hormone levels are top,1 with advanced,1 aberration,1 in uncontrolled diabetics.  The growth hormone may also caused hypertrophied kidneys in diabetic animal,1 or beastly,1.  Together with the furnishings,1 of insulin deficiency, ultimate basement membrane thickening may occur in the absence of leukocyte and phagocyte.[34]   
 
CHRONIC KIDNEY DISEASES AND DIET
 
Bladder dysfunction like neurogenic bladders are very common among diabetes patient with typical statistics of 25% cases among non-insulin-dependent diabetes mellitus (type II diabetes, NIDDM) and approximately 26-87% among patients of insulin-dependent diabetes mellitus (type I diabetes, IDDM).[26]  Typical analysis,1 maybe : (a) possible cavity,1 of the internal sphincter (b) 10-50 mg of bethanechol, three times a day in cholinergic therapy (c) long term alternate,1 or indwelling catheterization (d) ensure absolute,1 bladder emptiness with repetitive appointed,1 voiding every 3 to 4 hours.  The anticipation,1 of urinary tract infections among diabetic patients are comparatively higher than non-diabetics, that could be caused by fungus with counts greater than 104/mL on catheterized case,1 in typical primary infection.[27]   
Although there seemed no absolute,Gucci Sunglasses,1 correlations between diabetes mellitus or high blood glucose level and the fatal renal disease, certain altitude,1 of the kidneys could affect the calmness,1 of kidney problems.  Such relationships are also synonymous to diabetic nephropathy, Kimmelstiel-Wilson bane,1, diabetic renal disease or diabetic glomerulosclerosis.[5]  Three different mechanisms have been proposed for the bond,1 between the kidney and diabetes mellitus (1) arteriolosclerosis and arteriosclerosis (2) acute and chronic pyelonephritis (3) diabetic glomerulosclerosis per se.  Protein deposits on the endothelial aspects have confirmed the correlations.[6]  Initial changes are also found in the capillary basement membrane and mesangium that accrue,1 matrix and membrane-like material, leading to true birthmark,1 formation in lobular centre in nodular diabetic glomerulosclerosis.[7] 
11. Gardner K : Cystic Diseases of the Kidney.  John Wiley and Sons Inc.; 1976; United States of America; page 176
CONCLUSION
 
 
NEPHRONOPHTHISIS AND RENAL MEDULLARY CYSTIC DISEASE – CLINICAL MANIFESTATION
1.  Pyrah LN :  (1979) Renal calculus. Springer-Verlag; 1979; United Kingdom; page 18-20 
14. Axelsson U, Odlund B : Cystic disease of the renal medulla and its possible relation to juvenile nephronophitis.  Acta Med Scand; 1968; 183:275-280
 
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