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ARTICLE
Year : 1978  |  Volume : 24  |  Issue : 3  |  Page : 138-146

Diabetic nephropathy-a review


Department of Medicine, Seth G. S.Medical -College and K.E.M. Hospital, Parel, Bombay-400 012, India

Correspondence Address:
Vidya N Acharya
Department of Medicine, Seth G. S.Medical -College and K.E.M. Hospital, Parel, Bombay-400 012
India
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Source of Support: None, Conflict of Interest: None


PMID: 364042

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How to cite this article:
Acharya VN, Chawla KP. Diabetic nephropathy-a review. J Postgrad Med 1978;24:138-46

How to cite this URL:
Acharya VN, Chawla KP. Diabetic nephropathy-a review. J Postgrad Med [serial online] 1978 [cited 2019 May 20];24:138-46. Available from: http://www.jpgmonline.com/text.asp?1978/24/3/138/42658


Diabetic Nephropathy is a term used ti designate a syndrome, clinically manifested by varying combinations of protein uria, oedema, hypertension, azotaemi; and urinary tract infection. [78] It is a nephropathy of mixed aetiology to in elude degenerative and infectious processes which involve the renal parenchyma and contribute significantly to th( total disease.

The description of intercapillary glomerulosclerosis by Kimmelstiel and Wilson [38] in 1936 represented a historical landmark in the recognition and an understanding of the extent and character of chronic renal disease associated with diabetes. By this time it was 12 years since Banting and Best [8] had discovered Insulin enabling, diabetic patients to live for a longer time As years rolled by it was recognised that particularly in younger population, small vessel disease was the most common leading cause of death as opposed to large vessel disease in the middle aged and older population. [14],[40]


 :: Histopathology and Biochemistry Top


Intensive studies with light and elec­tron microscopy [69] has revealed that dia­betic nephropathy is a small vessel disease [5],[6],[7],[13],[16],[20],[41],[49],[50],[59],[60],[68],[69],[79] (micro-angiopathy) with complex clinic-pathological picture of diffuse and nodula glomerulosclerosis (DGS), often associated with chronic pyelonephritis, arterio and arteriolo-sclerosis. [6],[51],[78]

Before the description of intercapillary glomerulosclerosis, a process of glycogen nephrosis in the proximal tubule was first described by Armanni [4] and later by Ebstein [26] in 1882. Ritchie and Waugh [61] (1957) described this "glycogen nephrosis" as "Armanni and Ebstein diabetic nephropathy Kimmelstiel and Wilson [38] described the typical nodular lesion of glomerulosclerosis in autopsy studies in diabetic patients dying of advanced renal disease and called the clinical picture a. K.W. Syndrome. With the technique of renal biopsy [33],[36],[80] being made applic­able to the study of diabetes during life particularly after Insulin era, more ex­tensive study of early renal lesions it diabetics was made possible. Watkin, et al [76] have described results of a follow up renal biopsy studies in 1972. Thirty­one diabetic subjects on whom renal biopsies had been performed approxi­mately 11 years previously were re­viewed in order to determine the natu­ral history of diabetic renal disease over a long period. At the time of biopsy it was shown that neither renal function nor proteinuria was closely related to histo­logical changes. Although all the subjects with heavy proteinuria had advanced renal change, some patients with severe biopsy lesions had no proteinuria. When proteinuria was less in amount, the prognosis was variable, regardless of the histological change, and renal function sometimes remained unaltered for many years. All patients with heavy proteinuria and renal changes died during follow up.

In 1559 autopsy cases studied by Bell, [9] it was noted that below the age of 20 years, no glomerulosclerosis was seen. He further noted that when the duration of diabetes was less than 10 years, the incid­ence of DGS was 3%, when the duration was between 10-20 years, 50% showed DGS and when the duration was more than 20 years, almost 100% manifested DGS.

Combined biopsy and autopsy data has revealed that in DGS, three varieties of lesions [6],[21],[29],[58],[69],[76] viz. diffuse, nodular and exudative, are noted in the glomeruli, besides changes in the blood vessels and the interstitium. Mathur [52] et al (1964) in a study of 32 diabetic subjects with renal biopsy showed that 31 (96.9%) had defi­nite renal lesions. In their study it was noted that 71.9% of them had diffuse lesions, 12.4% had combined diffuse and exudative lesions and 6.2% had diffuse and nodular lesions. They also noted local­ised capillary dilatation of the glomerular tuft, forming aneurysms in 3 cases. This aneurysm formation [2],[3],[27],[32] is supposed to result secondary to obstruction of the blood flow resulting from the nodule.

Gupta and Chakravarty [33] in a study of 60 renal biopsies in 1964, noted changes of diabetic nephropathy in 30 (50%) of the cases. Very recently in 1975, Takazu­kura et al [71] from Japan have published their observations on the glomerular changes in diabetes by serial renal biopsy studies. They have concluded that diffuse, nodular and exudative lesions noted in the past are progressions of the same basic lesion seen in the glomeruli of diabetic kidneys. Gellman et a1 [29] classified the lesions into 4 grades. In grade I the lesion is local within each glomerulus and focal within each kidney. In grade II the mesangial thickening is diffuse within the glomerulus and generalised throughout the kidney. In grade III the capillary lumina are narrowed and only locally obliterated. An early nodular lesion ap­pears in the peripheral portion of the glomerular loop. In grade IV the luminar narrowing appears generally. The whole glomerulus becomes ischaemic and ap­pears hyalinised. The glomerulus contains a large nodular lesion.

Study of biochemical [65],[66],[67] aspect has re­vealed that in diabetes, abnormal quanti­ties of glycoproteins are formed from glucose in the absence of adequate Insulin to metabolise it. Mesangial cells are now recognised to play a major role in their production with involvement of the base­ment membrane of the glomeruli. [19] Due to the increased RNA production, both the renal size and renal function in­crease. [35],[44] The glycoprotein abnorma­lity in the glomerular basement mem­brane, as well as the increase in the renal growth have a common origin in an in­crease in the size of renal uridine tripho­sphate pool and/or its rate of formation. Considering the pathogenesis of diabetic nephropathy it is noted that early in its course, even when there is no evidence of clinical nephropathy, there is an increased insulin clearance and an increase in the GFR due to functional microangio­pathy. [6],[21],[23],[24],[46],[53],[54],[56] This results in an altered function of mesangial and en­dothelial cells. This, in turn, leads to the local accummulation of hyaline-PAS positive material which is either due to over production or decreased catabolism of glycoprotein with increase in the car­bohydrate content. Presently diffuse and exudative lesions that are noted in the glomeruli are considered to be one and the same process resulting from abnormal glycoprotein metabolism. [6],[21],[42]

In recent years, immunological mecha­nisms, [6],[12],[18],[28],[55] have been proposed as the responsible factors in the pathogenesis of diabetic micro-angiopathy. In DGS the glomerular basement membrane and the nodule have shown binding of fluorescent insulin, fluorescent antihuman globulin and fluorescent insulin antibodies. On the basis of these observations, the maturity onset diabetes is considered as an auto­immune disease with insulin as the res­ponsible antigen. Tubulo-interstitial disease noted in DGS may also have an autoimmune basis. Lot of further work is needed to confirm this hypothesis, as tubulo-interstitial auto-immunity is itself a concept of recent origin.

Epidemiological Data: Better control of diabetes with Insulin, diet and antidiabe­tic agents has markedly increased the life expectancy of diabetic patients. [6] The average duration of life in patients with the onset of diabetes below the age of 10 years, between 10-19 yrs. and between 20 to 39 yrs. has been reported to be 29.8 years, 26.7 years, and 27.2 yrs. respective­ly as compared to 1.3 years, 2.7 years and 4.3 years in the pre-insulin era. This has brought the consequence of diabetic micro-angiopathy in various organs to the forefront. Review of Western literature reveals that diabetic nephropathy is the most frequent cause of morbidity and mortality in patients with diabetes which has its onset early in life (below 40 years). [6],[11],[29],[76]

There is truly a paucity of observation on renal involvement in diabetes in our own country. There is no data available on the incidence of renal involvement in diabetes, inspite of the fact that quite a few diabetic clinics are functioning in many major cities. Vaishnava et al [72] in their study of diabetics in South India in an inpatient series found an incidence of renal lesions to be The duration of diabetes was less than 10 years in this group. Their observation was not repre­sentative of true incidence due to a very selective indoor population studied. Our own work from the Diabetic Clinic of the K.E.M. Hospital, Bombay comprising of a prospective data from a population of 372 outpatient diabetics indicated an in­cidence of renal involvement of 8.9% [1] Though the series was small yet it might represent what one would see in a mixed urban population.

Bell [10] in a study of 399 diabetics for vascular complications noted the incid­ence of nephropathy to be 10%. In dia­betes with vascular complications and with a disease of more than 15 years' dur­ation, it was found to be 34%.

Commenting on the clinico-pathological correlation, it is noted that diffuse, exuda­tive and nodular glomerular lesions, are all seen in DGS. Diffuse lesions however, were more frequent than the nodular ones, though the latter were more pa­thognomonic. In the light of newer under­standing of these being continuous pro­cesses, the rationale of this is easily dis­cernible. Though proteinuria may be ab­sent in the milder forms, it is a constant manifestation in severe type of nephro­pathy. [6],[21] Gellmen [29] has pointed out the fact that progressive worsening of clini­cal syndrome was better correlated with a diffuse lesion than that of the nodular form.

Observations of hypertension associated with diabetic nephropathy has been made by several authors. It is noted that arte­riosclerosis seems to have more significant relationship to hypertension than does either form of glomerulosclerosis. Bell [11] has commented that hyaline arteriosclero­sis is caused by diabetes and that hyper­tension is an effect of the arteriolar disease. A further marked correlation has been found between nodular lesion and the renal arteriolar hyalinisation. [69]

Asymptomatic bacteriuria, urinary tract infection and acute pyelonephritis are considered as a continuous process (continuum). Sathe et al, [62] in a study of 50 diabetic subjects from the diabetic clinic of the J.J. Group of Hospitals in 1960 noted an evidence of urinary tract infection in 32% of the subjects. This was before the introduction of the concept of "quantitative bacteriuria" and hence there could be .a large element of over­diagnosis in their work. Vaishnava [73] and his group have made some observations on this in 1974 but there appears to be a lot of confusion in the understanding of various. nomenclatures in their work. For the purpose of any definite observation, "significant baeteriuria" [37] has to be more than 1,00,000 organisms/ml. in 3 consecu­tive MSU samples or a growth of orga­nism from a single urine sample obtained by suprapubic bladder puncture. This alone would have 97 to 100% accuracy. Elsewhere in the congress we have report­ed an incidence of bacteriuria of 7.3% in an outpatient diabetic population of 302 subjects studied in a randomised fashion . [48] In this study it was noted that bacterial flora in the diabetics revealed a significant preponderance of gram positive organisms as compared to the pre-ponder­ance of E. coli in control subjects.

In Joslin Clinic [57] an incidence of 34/0 was noted in an inpatient population amongst 68 pateints consecutively admitted to The New England Deaconnes Flospital. This incidence was even higher (68%) in patients who had been confined to bed before admission.

After extensive studies, Vejlsgaard [74] has concluded that diabetic vascular disease was a contributory factor in the development of urinary tract infection in diabetes. Studies at Joslin Clinic have conclusively proved that bacteriuria and microangiopathy represented a particular hazard to pregnant diabetic women. [6]


 :: End Stage Diabetic Nephropathy Top


In a study of 1559 diabetic patients at autopsy, Bell [10] accounted for 5.3% of deaths as due to renal disease. Lundbaek [47] reported renal disease as a cause in 35% of patients with diabetes mellitus, diag­nosed before the age of 40 years and 12% diagnosed after 40 years of age. Warren et al [75] list 12% of 1036 deaths in diabetic patients at New England Deaconnes Hos­pital as due to renal failure. Over a 8 years' study, Joslin Clinic [6] reported 6800 deaths in diabetic patients. Renal involve­ment due to diabetes accounted for 6% of deaths in total population and almost 2/3rd diabetic deaths were due to diabetic nephropathy. Once diabetic renal lesion of grade III or so has set in, there is no effective treatment to slow down or change the course of diabetic renal failure. Until means are at hand to prevent dia­betic renal disease, it is pertinent on both the medical profession and the public to increase efforts to correct renal failure when it develops.

Rehabilitation of patients of end stage diabetic nephropathy with renal failure would involve regular dialysis treatment followed by renal transplantation. The diabetic patients have severe generalised vascular, retinal, metabolic and neurolo­gical disease, which precludes reason-able patient rehabilitation and survi­val. [15],[25],[30],[43],[63],[64],[65],[66],[67],[68],[69],[70],[71],[72],[73],[74],[75],[76],[77] Experience of workers at the Minneopolis Medical Research Foundation [63] has indicated that if any satisfactory results are to be obtained in diabetic patients, the dialysis has to be initiated when their average residual renal function and urine output are higher than they are in non-diabetic patients.

Diabetic patients do not tolerate severe renal insufficiency in the same manner as non diabetic patients, probably because of multisystem disease. [63] Effective rehabilit­ation is difficult to achieve in dialysed diabetic patients. Very few patients have been able to continue with their previous employment on dialysis.

Coming to the problem of renal trans­plantation, the Minnesota group [39] has had patients with juvenile onset insulin dependent diabetes, who have received transplants in 63 instances. Their figures indicate that these patients do worse than non-diabetic transplant patients. How­ever, these patients do even worse on dia­lysis as compared to cadaver donor trans­plantation. Post-operative urological com­plications are much more in this group as compared to non-diabetic patients. Late deaths caused by cardiovascular complic­ations and infections have dramatically worsened the prognosis of survival for diabetics with cadaver donor transplanta­tion. Certain groups of workers [31] have attempted heroic surgery of combined pancreatic and renal transplant with a view to offer simultaneous cure to both diabetes and renal failure. The results of these have not been encouraging so far. Thus for pure survival, live related donor kidney transplantation is the treatment of choice, whereas dialysis is the least suc­cessful choice of treatment. [39]

Certain groups of workers from U.S.A. [31] and Japan [17] have collected their cummulative experience with 15 patients treated with long term peritoneal dialysis. From their experience it is felt that he patients above the age of 40 years, where haemodialysis and renal transplantation are associated with poor prognosis and in those with cardiovascular disease, peri­toneal dialysis may offer successful pro­longation of life. This is particularly like­ly to succeed with stress on avoidance of chances of infection, with the use of Tenckhoff Silastic Catheter, a closed dia­lysate delivery system and rigid adher­ance to sterile technique. Thus a well motivated patient may achieve satisfac­tory rehabilitation while peritoneal dia­lysis is performed during sleep three to five nights per week.

Study of diabetic patients with success­ful transplants have shown marked im­provement in their physical well being, activity level, level of happiness, self image, degree of anxiety, level of sexual performance and in their marital and other relationship. [64] Successful pregnancy has been reported recently in a juvenile diabetic female after renal transplanta­tion. [70] This is certainly a small but cheer­ ful front in a gloomy outlook of patients with end stage diabetic nephropathy.

We, in our country have however, to step away from the romance of rehabilit­ation by dialysis and renal transplantation. which arouses our curiosity and accele­rates our sense of suspense to more basic problem of preventive management. It is worth spending maximum possible re­sources and finance on early detection of renal lesion, definitive and prolonged man­agement of urinary tract infection, and education of each diabetic patient and family regarding frequent and long term follow up to prevent these highly disabl­ing consequences of long term diabetes.

This alone would be a retional solution to the staggering cost of rehabilitation of patients of end stage renal disease.

 
 :: References Top

1.Acharya, V. N., Mamnani, K. V., Kulkarni, B. S., Sant, S. M. and Bhandarkar, S. D.: Study of renal in­volvement and renal insufficiency in diabetic subject. Paper presented at the Third National Congress on Diabetes held in Bombay in November, 1975.  Back to cited text no. 1    
2.Allen, C.: So called Int. Cap. glome­rulosclerosis lesion associated with dia­betes mellitus: Morphogenesis and signi­ficance. Arch. Path., 32: 33-51, 1941.  Back to cited text no. 2    
3.Anderson, G. S.: The pathogenesis of diabetic glomerulosclerosis. J. Path. and Bact., 67: 241-245, 1954.  Back to cited text no. 3    
4.Armanni: Quoted by Ebsteine, W.(1882) 26  Back to cited text no. 4    
5.Ashton, N.: Diabetic micro-angiopathy. Advances in Ophthalmol., 8: 1-84; 1958.  Back to cited text no. 5    
6.Balodimos, M. C.: "Diabetic Nephro­pathy". In Joslin's, `Diabetes Mellitus' 11th Edition; Editors-Marble, A., White, P., Bradley, R. F. and Krall, L. P. Lea, and Febiger Publishers, Philadelphia, 1971, pp. 526-561.  Back to cited text no. 6    
7.Balodimos, M. C.: Diabetic nephropathy and its relation to the micro-angiopathy of diabetes. latriki (Athens), 10: 540, 1966, as quoted by Balodimos [6] 1971 (pg. 526).  Back to cited text no. 7    
8.Banting, F. G. and Best C. H.: Pan­creatic extracts. J. Lab. & Clin. Med., 7: 464-472, 1922.  Back to cited text no. 8    
9.Bell, E. T.: A post-mortem study of vascular disease in diabetes, A. M. A. Arch. Path., 53: 444-453, 1952.  Back to cited text no. 9    
10.Bell, E. T.: Renal vascular disease in diabetic mellitus. Diabetes, 2: 376-389, 1953.  Back to cited text no. 10    
11.Bell, E. T.: "Diabetes mellitus: A clini­cal and pathological study of 2529 cases". Charles C. Thomas, Publishers: Spring­field, III, 1960, p. 35.  Back to cited text no. 11    
12.Berns, A. W., Owens, C. T., Hirata, Y. and Blumenthal, H. T.: The pathogenesis of diabetic glomerulosclerosis. II-A demonstration of insulin binding capacity of the various histopathological com­ponents of the disease by fluorescencemicroscopy. Diabetes, 11: 308-317, 1962.  Back to cited text no. 12    
13.Berkman, J. and Rifkin, H.: Newer aspects of diabetic micro-angiopathy. Ann. Rev. Med., 17: 83, 1966 as quoted by BalodimosC (pg. 526).  Back to cited text no. 13    
14.Blagg, C. R.: Visual and vascular pro­blems in dialyzed diabetic patients.Kidney International 6 (Suppl. 1): S-27 to S-31, 1974.  Back to cited text no. 14    
15.Blagg, C. R., Eschback, J. W., Sawyer, T. K. and Casbaretto, A. A.: Dialysis for end stage diabetic nephropathy. Proc. Dialysis Transplant Forum, 1: 133-135, 1971.  Back to cited text no. 15    
16.Bloodworth, J. M. B. Jr.: Diabetic microangiopathy. Diabetes, 12: 99-114, 1963.  Back to cited text no. 16    
17.Blumenkrantz, M. J., Shapiro, D. J., Mimura, N., Oreopaulus, D. G., Friedler, R. M., Levin, S., Tenckhoff, H. and Coburn, J. W.: Maintenance of peri­toneal dialysis as an alternative in the patients with diabetes mellitus and end stage uremia. Kidney International. 6 (.Suppl. 1) : S-108 to S-114, 1974.  Back to cited text no. 17    
18.Blumenthal, H. T., Hirata, Y., Owens, C. T. and Berns, A. W.: Histologic and immunologic analysis of the small vessels­lesions of diabetes in the human and in the rabbit. In, "Small blood vessels in Diabetes Mellitus" Editors-Siperstein, M. P., Colwell, A. R. Sr. and Meyer, K., American Institute of Biological Sciences, Washington, 1964, p. 279.  Back to cited text no. 18    
19.Cahill, G. F. Jr.: Summary of the 13th Research Symposium on "Perspective in Current Diabetic Research". Diabetes, 24: 1123-1124, 1975.  Back to cited text no. 19    
20.Costanzi, G., Manchini, A. M., Zampa, G. A. and Kelescian, G.: Recent studies aquisizion, Sulke lesions, microvascolovi in corso di diabete mellitus. Recent Progr. Med. (Roma.), 40: 89, 1966 as quoted by Balodimos. [6] (pg. 523).  Back to cited text no. 20    
21.Churg, J. and Dolger, H.: Diabetic renal disease. In, "Diseases of the kidney" 2nd Edition-Editors-Strains and Welt. Little Brown & Co., Boston, 1971, p. 873­889.  Back to cited text no. 21    
22.Churg, J. and Pacts, J.: Diabetic renal disease-Arteriosclerosis and glomerulos­clerosis. In, "Pathology Annual" Editor­ Sommers, S. C.. Appleton, Century Crofts, New York, 1966.  Back to cited text no. 22    
23.Ditzel, J.: Functional microangiopathy it diabetes mellitus. Diabetes, 17: 388-397, 1968.  Back to cited text no. 23    
24.Ditzel, J. and Junker, K.: Abnormal glomerular filtration rate, renal plasma flow and renal proteins excretion in recent and short term diabetes. Brit. Med. J., 2: 13-19, 1972.  Back to cited text no. 24    
25.Drukker, W., Haag-sma-schouten, W. A. G., Alberts, C. H. A. and Baarda, B.: Report on regular dialysis treatment in Europe VI, 1970. Proc. Sur. Dialysis Transplant Assoc., 7: 3-14, 1970.  Back to cited text no. 25    
26.Ebsteine, W.: Weiteres uber diabetes mellitus insbesondere uber die complica­tion deselber mit Typhus abdominalis. Deutsches Arch. f. Klin. Med. 30: 1-44; 1882, As quoted by Ritchie and Waugh (1957). [61]   Back to cited text no. 26    
27.Fahr, T.: Uber glomerulosklerose. Vir­chow's. Arch. Path. Anat., 309: 16-33, 1942.  Back to cited text no. 27    
28.Farrant, P. C. and Shedden, W. 1. H.: Observation on the uptake of insulin con­jugated with fluorescent isothiocyanate by diabetic kidney tissue. Diabetes, 14: 274-278, 1965.  Back to cited text no. 28    
29.Gellman, D. D., Pirrani, C. L., Soothill, J. F.: Muehrcke, R. C. and Kark, R. M.: Diabetic nephropathy-A clinical and pathologic study based on renal biopsies. Medicine, 38: 321-367. 1959.  Back to cited text no. 29    
30.Ghavamian, M. Gutch, C. F., Kopp, K. F. and Kolfl, W. J.: The sad truth about hemodialysis in diabetic nephropathy. J. Amer. Med. Assoc., 222: 1386-1389, 1972.  Back to cited text no. 30    
31.Gliedman, M. L., Tellis, V., Soberman, R., Rifkin, H.. Freed, S. Z. and Veith, F. J.: Pancreatic transplantation in New York. Kidney International. 6 (Suppl. 1): S-164 to S-168, 1974.  Back to cited text no. 31    
32.Gunther, W. H. (1941): Quoted by Anderson-3 (1954).  Back to cited text no. 32    
33.Gupta, J. K. and Chakravarty, S. N.: Renal lesion in diabetic mellitus. J. Assoc. Phy. India. 12: 547-555, 1964.  Back to cited text no. 33    
34.Iversen, P. and Brun- C.: Aspiration biopsy of the kidney. Amer. J. Med., I1: 324-330, 1951.  Back to cited text no. 34    
35.Kahn, C. B., Raman, P. G. and Zic, Z.:Kidney size in diabetes-mellitus. Dia­betes, 23: 788-792; 1974.  Back to cited text no. 35    
36.Kark, R. M., Muehreke, R. C . , Pollak,V. E., Pirani, C. L. and Diefer, J. H.:An analysis of five hundred percutaneous renal biopsies. Arch. Intern. Med., 101:439-451, 1958.  Back to cited text no. 36    
37.Kass, E. H.: Pathogenesis of pyelone­phritis. In, "The kidney", Editors­ Mostofi, F. K. and Smith, D. E., Inter­national Academy of Pathology, Mono­graph No. 6, Williams and Wilkins, Batli­more, 1966, p . 204.  Back to cited text no. 37    
38.Kimmelstiel, P. and Wilson, C.: Inter­capillary lesions in the glomeruli of the kidney. Amer. J. Path., 12: 83-97, 1936.  Back to cited text no. 38    
39.Kjellstrand, C. M . , Shideman, J. R.,Simmons, R. L., Buselmeier, T. J., Hartlitzsch, Goetz, F. C. and Najarian, J. S.: Renal transplantation in insulin dependent diabetic patients. Kidney In­ternational. 6 (Suppl. 1): S-15 to S-20, 1974.  Back to cited text no. 39    
40.Knowles, H. C. Jr.: Magnitude of the renal failure problem in diabetic nephro­pathy. Kidney International. 6 (Sup. 1): S-2 to S-7, 1974.  Back to cited text no. 40    
41.Latotzki, H.: Probleme der diabetischen kapillaropathie insbesondere der dia­betischen nephropathie als spatkomplika­tionen der zuckerkrankheit. Aerztl Fort­bild, 58: 1157-1163, 1964.  Back to cited text no. 41    
42.Lazyarow, A. and Speidel, E.: The chemical composition of the glomerular basement membrane and its relationship to the production of diabetic complica­tions. In, "Small blood vessel involvement in diabetes mellitus". Editors-Serpan­stein, M. A., Golwell, A. P. Sr. and Meyer, K.: American Institute of Biologi­cal Sciences, Washington, D . C . , 1964, p. 127.  Back to cited text no. 42    
43.Leonard, A., Comty, C., Raij, L., Rat­tazzi T., Wathen, R. and Shapiro, F. L.: The natural history of regularly dialyzed ­diabetics. Trans. Amer. Soc. Artif. Intern. Organs ., 19: 282-286, 1973.  Back to cited text no. 43    
44.Levin, N. W., Cortes P., Silveira, E. and Rubenstein, A. H Relation of renal growth to diabetic glomerulosclerosis. Lancet, 2: 1120-1121, 1975.  Back to cited text no. 44    
45.Loube, S. D.: The microangiopathy of diabetes. Med. Ann. D.C., 33: 9-14, 1964.  Back to cited text no. 45    
46.Lundbaek, K. Mogenson. C. E. and Anderson, N. J. F.: Increased kidney size and glomerular filtration rate in un­treated juvenile diabetics: Normalisation by strict insulin treatment. (Abstract) Diabetologia, 10: 378, 1974.  Back to cited text no. 46    
47.Lundbaek, K.: Nephropathy in diabetic subjects. In, "The nature and treatment of Diabetes". Editors-Leibel, B. S., Wrenshall, G. A. Excerpta Medica Foundation New York, 1965, pp. 436-446.  Back to cited text no. 47    
48.Mamnani, K. V . , Jadhav, Surangi. Bhandarkar, S. D. and Acharya Vidya, N.: Pattern of Urinary tract infection in diabetic subjects; Presented at the Third National Congress on Diabetes held in Bombay in November, 1975.  Back to cited text no. 48    
49.Marble, A.: Diabetic Nephropathy. J. Clin. Endocrinolol., 15: 399, 1955 as quoted by Rifkin and Berkman. [58]   Back to cited text no. 49    
50.Marble, A.: Angiopathy in Diabetes-An unsolved problem, Diabetes, 16: 825 838, 1967.  Back to cited text no. 50    
51.Marble, A., Wilson, J. L. and Root, H. F.: Diabetic Nephropathy. A clinical syndrome. Trans. Assoc. Amer. Physi­cians, 64: 353, 1951 as quoted by Rifkin and Berkman. [58]  Back to cited text no. 51    
52. Mathur, K. S., Wahi, P. N., Gunta, 0. P. and Mathur. C. P.: Diabetic Naphro­pathy-A clinical and histological study by renal biopsy. J. Assoc. Phys. India, 12: 535-546, 1964.  Back to cited text no. 52    
53.Mogenson, C. E.: Glomerular filtration rate and renal plasma flow in short term and long term juvenile diabetes. Scand. J. Clin. Lab. Invest., 28: 91-100, 1971.  Back to cited text no. 53    
54.Mogenson, C. E. and Anderson, M. J. F.: Increased kidney size and glomerular filtration rate in early juvenile diabetes. Diabetes, 22: 706-712. 1973.  Back to cited text no. 54    
55.Pav, J., Jezkova, Z. and Skrha, F.: In­sulin antibodies. Lancet, 2: 221-223, 1963.  Back to cited text no. 55    
56.Randerath, E.: Zur Frage der intereapil­laren (diabetischen) glomerulosklerose. Virchow's Arch. Path. Anat. 323: 483­523, 1953.  Back to cited text no. 56    
57.Rengart, R. T.: A symptomatic bacilluria in sixty-eight diabetic patients. Amer. J. Med. Sci. 239: 159-164, 1960.  Back to cited text no. 57    
58.Rifkin, H. and Berkman, J.: ' - Diabetic and the kidney. In, "Diabetic mellitus". Theory and Practice (Editors: Ellenberg M. and Rifkin H. J.) McGraw-Hill Book Company, 1970, pg. 848.  Back to cited text no. 58    
59.Rifkin, H. and Leiter, L.: Diabetic microangiopathy. New York J. Med.,61: 1920, 1961 as quoted by Balodimos,s pg. 526.  Back to cited text no. 59    
60.Rifkin, H., Leiter, L. and Berkman, J.: Current concepts of diabetic microangio­pathy. Advances Intern. Med., 11: 235, 1963, as quoted by Balodimos,O pg. 526.  Back to cited text no. 60    
61.Ritchie, S. and Waugh, D.: The patho­logy of Armanni Ebstein diabetic nephro­pathy. Amer. J. Path. 33: 1035-1037, 1957.  Back to cited text no. 61    
62.Sathe, R. V., Talwalkar, N. G. and Rath, G. S.: Urinary tract infection in diabetes mellitus. J. Assoc. Phys. India, 8: 307-310, 1960.  Back to cited text no. 62    
63.Shapiro, F. L., Leonard, A. and Comty, C. M.: Mortality, morbidity and rehabi­litation results in regularly dialyzed patients with diabetes mellitus. Kidney International, 6 (Suppl. 1): S-8 to S-14, 1974.  Back to cited text no. 63    
64.Simmons, R. G. and Schilling, K.: Social and psychological rehabilitation of the diabetic transplant patient. Kidney International, 6 (Suppl. 1): S-152 to S-158, 1974.  Back to cited text no. 64    
65.Spiro, R. G.: Glycoproteins and diabetes. Diabetes, 12: 223-230, 1953.  Back to cited text no. 65    
66.Spiro, R. G.: The structure of the di­saccharide units of the renal glomerular basement membrane. J. Biol. Chem., 242: 4813-4823, 1967.  Back to cited text no. 66    
67.Spiro, R. G.: Chemistry of the renal glomerular basement membrane in dia­betes, Proc. 6th Intern. Diabetes Federa­tion, Stockholm 1967. Excerpta Medica Foundation, J. Ostman (Ed.), Amster­dam, 1969, pg. 586.  Back to cited text no. 67    
68.Stary, H. C.: Diseases of small blood vessels in diabetes mellitus. Amer. J. Med. Sci., 252: 357-374, 1966.  Back to cited text no. 68    
69.OSterby, R.: Early phases in the develop­ment of diabetic glomerulopathy. Quan­titative electromicroscopic study. Acta. Med. Scandinav., (Suppl. 574), 1975, pg. 54.  Back to cited text no. 69    
70.Tagatz, G. E., Neil I. A., Goetz, F. C., Najarian, J. S. and Simmons, R. L.: Pregnancy in a juvenile diabetic after renal transplantation (Class T-Diabetes mellitus). Diabetes, 24: 497501, 1975.  Back to cited text no. 70    
71.Takazakura, E., Nakamoto, Y. Hayakawa, H., Kawai, K., Muramoto, S., Yoshida, K., Shimizu, M., Shinoda, A., Takeuchi, J. and Kanazawa: Onset and progression of diabetic glomerulosclerosis. Diabetes, 24: 1-9, 1975.  Back to cited text no. 71    
72.Vaishnava, H., Dixit, N. S. and Soloman, S. K.: Study of diabetes in South India. J. Assoc. Phys. India, 12: 255-276, 1964.  Back to cited text no. 72    
73.Vaishnava, H., Rizvi, S. N. A., Govil, H. C., Dixit, N. S. and Gulati, P. D.: A symptomatic kidney and urinary tract infection in Indian diabetic. J. Assoc. Phys. India, 22: 309-312, 1974.  Back to cited text no. 73    
74.Vajlsgaard, R.: Significant bacteriuria in relation to vascular disease of diabetes of long duration. In, "Progress in Pyelone-­phritis". Editor-Kass, E. H., F. A. Davis Co., Philadelphia, 1965. p. 492.  Back to cited text no. 74    
75.Warren, S., Le Compte, P. M. and Legg, M. A.: "Pathology of diabetic mellitus", 4th Ed., Lea and Febiger, Philadelphia, 1966, pg. 227.  Back to cited text no. 75    
76.Watkins, P. G., Blainey, J. D., Brewer, D. B., Fitzgerald, M. G., Malins, J. M., O'Sullivan, D. T. and Pinto, J. A.: The natural history of diabetic renal disease. Quart. J. Med., 41: 437-456, 1972.  Back to cited text no. 76    
77.White, N., Snowden, S. A., Parson, V., Sheldon, J. and Bewick, M.: The manage­ment of terminal renal failure in diabetic patients by regular dialysis therapy. Nephron, 11: 261-275, 1973.  Back to cited text no. 77    
78.Wilson, J. L., Root, H. F. and Marble, A.: Diabetic Nephropathy. A clinical syndrome. New Eng. J. Med. 24.5: 513­517, 1951.  Back to cited text no. 78    
79.Winegrad, A. 1. and Burden, C. L.: 1­Xylose metabolism in diabetes mellitus. New Eng. J. Med., 274: 298-305, 1966.  Back to cited text no. 79    
80.Wolstenholme, G. E. W. and Cameron, M. P.: "Renal Biopsy"-A Ciba founda­tion: Symposium. Little, Brown and Co., Boston, 1962.  Back to cited text no. 80    




 

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