Chapter 1 commencing feedback (pages 1–3): Arnold R. Rich
Chapter 2 Ultrastructure of the Glomerulus and adjustments in high quality constitution linked to elevated Permeability of the Glomerulus to Protein (pages 4–31): Robert L. Vernier
Chapter three Glomerular harm by way of “Pore measurement” (pages 32–50): J. Hardwicke and J. F. Soothill
Chapter four Electron Microscopy of Renal Glomerular Amyloidosis (pages 51–69): A. Bergstrand and H. Bucht
Chapter five medical, Microscopic and Electron Microscopic information within the Nephrotic Syndrome of Unknown beginning (pages 70–102): R. Habib, P. Michielsen, E. De Montera, N. Hinglais, P. Galle and J. Hamburger
Chapter 6 The high quality constitution of the Glomerulus in Bright's sickness: A Clinico?Pathological research (pages 103–155): Henry Z. Movat, Jan W. Steiner and Robert J. Slater
Chapter 7 Post?Streptococcal Glomerulonephritis (pages 156–193): David P. Earle and Robert B. Jennings
Chapter eight Focal Glomerulonephritis (pages 194–217): R. H. Heptinstall and A. M. Joekes
Chapter nine Lupus Nephritis (pages 218–244): Conrad L. Pirani, Victor E. Pollak, Robert C. Muehrcke and Robert M. Kark
Chapter 10 Percutaneous Renal Biopsy in Pyelonephritis (pages 245–261): Claus Brun and Flemming Raaschou
Chapter eleven Correlation among Renal Biopsy and different Diagnostic methods in Pyelonephritis (pages 262–280): M. S. R. Hutt and H. E. De Wardener
Chapter 12 the importance of Renal Biopsy for the prognosis of Pyelonephritis in Diabetic sufferers (pages 281–308): Age Chr. Thomsen
Chapter thirteen Quantitative Histochemistry of the Nephron (pages 309–329): Robert M. Kark, Hermann Mattenheimer, Sjoerd L. Bonting, Victor E. Pollak and Robert C. Muehrcke
Chapter 14 a few Observations at the high quality constitution of Human Kidney Biopsies in Acute Anuria and Osmotic Diuresis (pages 330–378): O. Z. Dalgaard and okay. J. Pedersen
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Extra resources for Ciba Foundation Symposium - Renal Biopsy: Clincal and Pathological Significance
46 DISCUSSION I have great difficulty in reconciling what I have seen in the microscope with what Dr. Pirani, Dr. Jennings, and Dr. Slater mentioned; that is, patients with severe proteinuria, in whom the epithelial cell morphology is entirely different from that in our group of patients with severe proteinuria. Do some nephrotic patients have tubular proteinuria ? In this case the glomerulus might well look different. Hardwicke: I carefully avoided saying anything about the aetiology of proteinuria in these cases which we call “primarily renal disease”.
There was no correlation between the severity of the primary disease and renal impairment. The Congo red retention test showed only slightly pathological values, probably because there were no signs of generalized amyloidosis. Thus no extrarenal amyloid was found in liver biopsies (no. 26, 3 5 , I 53) or at autopsy (no. 73). None of the patients showed a nephrotic syndrome at the time of the investigation. Patient no. 26, however, died a few months after the last examination from a severe nephrotic syndrome with uraemia.
4; a very satisfactory linear relatioiiship is found. 6 (Malmendier, Gregoire and Lambert, 1957) (Pappenheimer, 1955) (Monke and Yuile, 1940) (Phelps and Putnam, 1960) these are included in Fig. 4. Once again the relationship between molecular weight and clearance is demonstrated; the data suggest a regression parallel with that for dextran, but suggesting that protein molecules are excreted slightly more readily than a dextran of equivalent molecular weight ; when, however, the same data are plotted on the basis of reciprocal of diffusion constant (a figure which might be expected to be more closely correlated with passage through capillary membranes), an equally good fit is obtained (Fig.