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Time course of the pulmonary function parameters: (a) forced vital capacity and (b) forced expiratory volume in first second.
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fig1
Graft function was untainted during this incident, and the patient's pulmonary function parameters were satisfactory (Table 1 and Figures 1(a) and 1(b)).
Time course of serum creatinine (mg/dL) and proteinuria, respectively. Urinary protein excretion measured by +-urinary dip stick (mg) and  protein/creatinine ratio (mg/g).
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fig2
Notably, before her presentation in 2006, the renal function was normal, and there was no evidence of proteinuria or hematuria (Figure 2). 
Electron microscopical changes in kidney (a) and native lung (b) biopsies. Glomerular podocytes (P) show extensive accumulation of "myeloid" and "zebroid" bodies (arrows) characteristics of Fabry diseases. However, capillary loops (CL) remain open, and endothelial cells (E) do not exhibit morphological changes. Ciliated pulmonary epithelial cells show an increase and accumulation of irregularly shaped inclusions in lysosomes and autophagosomes consistent with storage of sphingolipids (arrows).
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fig3
A renal biopsy revealed the definite histological diagnosis of Fabry disease of the kidney (Figure 3(a)).  Most areas did not exhibit specific pathological changes; however, in some ciliated cells, an accumulation of autophagic or "myeloid-like" inclusion bodies was seen (Figure 3(b)).
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Pedigree. Latin letters indicate generations;   indicates affected males;   indicates unaffected males;   indicates unaffected females;   indicates unaffected females;   indicates no children; // indicates divorce; b.: year of birth; AGAL: alpha-galactosidase A activity; GLA: respective GLA mutation.
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fig4
The pedigree of the family is depicted in detail in Figure 4.
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